Inflammatory Disorders of Heart

Question 1

Infective endocarditis (IE)

Answer 1

is an infection of the endocardial layer of the heart.

Question 2

IE The subacute form

Answer 2

affects those with preexisting valve disease and has a clinical course that may extend over months.

Question 3

IE acute form

Answer 3

affects those with healthy valves and manifests as a rapidly progressive illness.

Question 4

The most common causative organisms of IE

Answer 4

Staphylococcus aureus and Streptococcus viridans, are bacterial. Other possible pathogens include fungi and viruses

Question 5

IE Etiology and Pathophysiology

Answer 5

occurs when blood flow within the heart allows the causative organism to infect previously damaged valves or other endothelial surfaces.

Question 6

Risk Factors for Endocarditis Cardiac Conditions

Answer 6

• Prior endocarditis • Prosthetic heart valve(s) • Acquired valve disease (e.g., mitral valve prolapse with regurgitation, calcified aortic stenosis) • Heart lesions (e.g., ventricular septal defect, asymmetric septal hypertrophy) • Rheumatic heart disease (e.g., mitral valve regurgitation) • Congenital heart disease • Pacemaker • Marfan’s syndrome • Cardiomyopathy

Question 7

Risk Factors for Endocarditis Noncardiac Conditions

Answer 7

• Hospital-acquired bacteremia • IV drug abuse

Question 8

Risk Factors for Endocarditis

Procedure-Associated Risks

Answer 8

• Intravascular devices (e.g., central venous catheter)

Question 9

Vegetations

Answer 9

the primary lesions of IE, consist of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium. The loss of parts of these fragile vegetations into the circulation results in emboli.

Question 10

IE disease progression

Answer 10

The infection may spread locally and damage the valves or their supporting structures. This causes dysrhythmias, valve dysfunction, and eventual invasion of the myocardium, leading to heart failure (HF), sepsis, and heart block

Question 11

The main contributing factors to IE include

Answer 11

(1) aging (more than 50% of older people have calcified aortic stenosis [AS]), (2) IVDA, (3) use of prosthetic valves, (4) use of intravascular devices resulting in health care–associated infections (e.g., methicillin-resistant S. aureus [MRSA]), and (5) renal dialysis.

Question 12

The clinical manifestations of IE

Answer 12

fever, chills, weakness, malaise, fatigue, and anorexia. Arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, and clubbing of fingers may occur in subacute forms of IE. Fever may be absent in older adults or those who are immunocompromised.

Question 13

Vascular signs of IE include

Answer 13

splinter hemorrhages, (black longitudinal streaks) that may occur in the nail beds.
Petechiae may result from fragmentation and microembolization of vegetative lesions.
Osler’s nodes
Janeway’s lesions

Question 14

Osler’s nodes

Answer 14

(painful, tender, red or purple, pea-size lesions) may be found on the fingertips or toes.

Question 15

Janeway’s lesions

Answer 15

(flat, painless, small, red spots) may be seen on the fingertips, palms, soles of feet, and toes.

Question 16

Roth’s spots.

Answer 16

Eye examination may reveal hemorrhagic retinal lesions

Question 17

Murmurs

Answer 17

The onset of a new or worsening systolic murmur is noted in most patients with IE. The aortic and mitral valves are most often affected.

Question 18

patient’s health history

Answer 18

Ask patients if they have had any recent (within the past 3 to 6 months) dental, urologic, surgical, or gynecologic procedures, including normal or abnormal obstetric delivery. Note any previous history of IVDA, heart disease, recent heart catheterization, heart surgery, intravascular device placement, renal dialysis, or infections (e.g., skin, respiratory, urinary tract).

Question 19

IE Diagnostic Studies

Answer 19

Three blood cultures drawn over a period of 1 hour from three different sites will be positive in most patients.3 Culture-negative endocarditis is often associated with antibiotic usage within the previous 2 weeks, or results from a pathogen not easily detected by standard culture tests. Cultures that are negative should be kept for 3 weeks if the clinical diagnosis remains IE because of the possibility of slow-growing organisms. A mild leukocytosis occurs in acute IE (uncommon in subacute). The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels may also be elevated.

Question 20

Major criteria to diagnose IE include at least two of the following:

Answer 20

two positive blood cultures 12 hours apart, nonvalvular regurgitation,
or intracardiac mass or vegetation noted on echocardiography

Question 21

Target Groups for Prophylactic Antibiotics

Answer 21

• Prosthetic heart valve or prosthetic material used to repair heart valve • Previous history of infectious endocarditis • Congenital heart disease (CHD)* • Unrepaired cyanotic CHD (including palliative shunts and conduits) • Repaired congenital heart defect with prosthetic material or device for 6 mo after the procedure • Repaired CHD with residual defects at the site or adjacent to the site of prosthetic patch or prosthetic device • Heart transplantation recipients who develop heart valve disease

Question 22

Conditions or Procedures Requiring Antibiotic Prophylaxis

Answer 22

• Oral • Dental manipulation involving the gums or roots of the teeth • Dental manipulation involving puncture of the oral mucosa • Respiratory • Respiratory tract incisions (e.g., biopsy) • Tonsillectomy and adenoidectomy • Surgery • Procedures that involve infected skin, skin structures, or musculoskeletal tissue

Question 23

IE Drug Therapy goals

Answer 23

Accurate identification of the causative organism is the key to successful treatment of IE. Long-term treatment is necessary to kill dormant bacteria within the valvular vegetations. Complete removal of the organism generally takes weeks, and relapses are common.

Question 24

The effectiveness of therapy is assessed with

Answer 24

subsequent blood cultures. Cultures that remain positive indicate inadequate or inappropriate selection of antibiotic, aortic root or myocardial abscess, or the wrong diagnosis (e.g., an infection elsewhere).

Question 25

Nursing Assessment Infective Endocarditis Subjective Data Important Health Information

Answer 25

Past health history: Valvular, congenital, or syphilitic heart disease, including valve repair or replacement. Previous endocarditis, childbirth, staphylococcal or streptococcal infections, hospital-acquired bacteremia Medications: Immunosuppressive therapy Surgery or other treatments: Recent obstetric or gynecologic procedures. Invasive procedures, including catheterization, cystoscopy. Recent dental or surgical procedures, GI procedures (e.g., endoscopy)

Question 26

Nursing Assessment Infective Endocarditis Subjective Data Functional Health Patterns

Answer 26

Health perception–health management: IV drug abuse, alcohol abuse. Malaise Nutritional-metabolic: Weight gain or loss, anorexia. Chills, diaphoresis Elimination: Bloody urine Activity-exercise: Exercise intolerance, generalized weakness, fatigue. Cough, dyspnea on exertion, orthopnea, palpitations Sleep-rest: Night sweats Cognitive-perceptual: Chest, back, or abdominal pain. Headache, joint tenderness, muscle tenderness

Question 27

Nursing Assessment Infective Endocarditis Objective Data

Answer 27

Fever, Osler’s nodes on extremities, splinter hemorrhages under nail beds, Janeway’s lesions on fingertips, palms, soles of feet, and toes. Petechiae of skin, mucous membranes, or conjunctivae. Purpura, peripheral edema, finger clubbing, Tachypnea, crackles, Dysrhythmia, tachycardia, new murmurs, S3, S4. Retinal hemorrhages

Question 28

Nursing Assessment Infective Endocarditis

Possible Diagnostic Findings

Answer 28

Leukocytosis, anemia, ↑ ESR, ↑ CRP and cardiac biomarkers. Positive blood cultures, hematuria. Echocardiogram showing chamber enlargement, valvular dysfunction, and vegetations. Chest x-ray showing cardiomegaly and pulmonary infiltrates. ECG demonstrating ischemia and conduction defects. Signs of systemic embolization or pulmonary embolism

Question 29

Arthralgia is common in IE.

Answer 29

Assess the patient for joint tenderness, decreased range of motion (ROM), and muscle tenderness. Examine the patient for petechiae, splinter hemorrhages, and Osler’s nodes.

Question 30

Nursing Diagnoses IE

Answer 30

• Decreased cardiac output related to altered heart rhythm, valvular insufficiency, and fluid overload
• Activity intolerance related to generalized weakness, arthralgia, and alteration in O2 transport secondary to valvular dysfunction

Question 31

The overall goals for the patient with IE include

Answer 31

(1) normal or baseline heart function, (2) performance of activities of daily living (ADLs) without fatigue, and (3) knowledge of the therapeutic regimen to prevent recurrence of endocarditis.

Question 32

Teaching the patient at high risk for IE

Answer 32

Tell the patient to avoid people with infections, especially upper respiratory tract infections, and to report cold, flu, and cough symptoms. Stress the importance of avoiding excessive fatigue, and the need to plan rest periods before and after activity. Good oral hygiene, including daily care and regular dental visits, is critical. Be certain the patient understands the importance of prophylactic antibiotic therapy before certain invasive procedures. Refer the patient with a history of IVDA for drug rehabilitation.

Question 33

Evaluation IE

Answer 33

• Maintain adequate tissue and organ perfusion
• Maintain normal body temperature
• Report an increase in physical and emotional comfort

Question 34

Acute Pericarditis

Answer 34

condition caused by inflammation of the pericardial sac (pericardium).

Question 35

Common Causes of Pericarditis Infectious

Answer 35

• Viral: Coxsackie A and B virus, echovirus, adenovirus, mumps, hepatitis, Epstein-Barr, varicella zoster, human immunodeficiency virus • Bacterial: Pneumococci, staphylococci, streptococci, Neisseria gonorrhoeae, Legionella pneumophila, Mycobacterium tuberculosis, septicemia from gram-negative organisms • Fungal: Histoplasma, Candida species • Others: Toxoplasmosis, Lyme disease

Question 36

Common Causes of Pericarditis Noninfectious

Answer 36

• Renal failure • Acute myocardial infarction • Neoplasms: Lung cancer, breast cancer, leukemia, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma • Trauma: Thoracic surgery, pacemaker insertion, cardiac diagnostic procedures • Radiation • Dissecting aortic aneurysm • Myxedema

Question 37

Common Causes of Pericarditis Hypersensitive or Autoimmune

Answer 37

• Dressler syndrome • Postpericardiotomy syndrome • Rheumatic fever • Drug reactions (e.g., procainamide, hydralazine) • Rheumatologic diseases: Rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis (scleroderma), ankylosing spondylitis

Question 38

Pericarditis in the patient with an MI may be described as two distinct syndromes.

Answer 38

• The first is acute pericarditis, which may occur within the first 48 to 72 hours after an MI.
• The second is Dressler syndrome (late pericarditis), which occurs 4 to 6 weeks after an MI

Question 39

characteristic pathologic finding in acute pericarditis.

Answer 39

An inflammatory response is the characteristic pathologic finding in acute pericarditis. There is an influx of neutrophils, increased pericardial vascularity, and eventually fibrin deposition on the epicardium

Question 40

Clinical Manifestations In acute pericarditis, clinical symptoms include

Answer 40

progressive, frequently severe, sharp chest pain. The pain is generally worse with deep inspiration and when lying flat. It is relieved by sitting up and leaning forward. The pain may radiate to the neck, arms, or left shoulder, making it difficult to differentiate from angina.

Question 41

One distinction is that the pain from pericarditis can be referred to the

Answer 41

trapezius muscle (shoulder, upper back). The dyspnea that accompanies acute pericarditis is related to the patient’s need to breathe in rapid, shallow breaths to avoid chest pain. Dyspnea may be aggravated by fever and anxiety.

Question 42

** The hallmark finding in acute pericarditis is

Answer 42

the pericardial friction rub. The rub is a scratching, grating, high-pitched sound believed to result from friction between the roughened pericardial and epicardial surfaces.

Question 43

pericardial friction rub diagnosis

Answer 43

It is best heard with the stethoscope placed at the lower left sternal border of the chest with the patient leaning forward.

Question 44

pericardial friction rub pt assessment

Answer 44

Since it is difficult to tell a pericardial friction rub from a pleural friction rub, ask the patient to hold his or her breath. If you still hear the rub, then it is cardiac. Pericardial friction rubs may require frequent attempts to identify because they are often intermittent and short lived.

Question 45

Two major complications that may result from acute pericarditis are

Answer 45

pericardial effusion and cardiac tamponade.

Question 46

Pericardial effusion

Answer 46

is a build-up of fluid in the pericardium. It can occur rapidly (e.g., chest trauma) or slowly (e.g., tuberculosis peri­carditis). Large effusions may compress nearby structures. Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. Phrenic nerve compression can cause hiccups, and compression of the laryngeal nerve may result in hoarseness. Heart sounds are generally distant and muffled, although BP is usually maintained.

Question 47

Cardiac tamponade

Answer 47

develops as the pericardial effusion increases in volume. This results in compression of the heart. The speed of fluid accumulation affects the severity of clinical manifestations. Cardiac tamponade can occur acutely (e.g., rupture of heart, trauma) or subacutely (e.g., secondary to renal failure, malignancy).

Question 48

The patient with cardiac tamponade may report

Answer 48

chest pain and is often confused, anxious, and restless. As the compression of the heart increases, there is decreased cardiac output (CO), muffled heart sounds, and narrowed pulse pressure. The patient develops tachypnea and tachycardia. Neck veins are usually markedly distended because of increased jugular venous pressure.