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CH 36 Inflammatory and Structural Heart Disorders Flashcards

1
Q

is a disease of the endocardial layer of the heart.

A

Infective endocarditis (IE)

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2
Q

is the innermost layer of the heart and heart valves

A

endocardium

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3
Q

most often affects the aortic and mitral valves

A

IE (Infective endocarditis)

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4
Q

(e.g., IV drug use IE [IVDA IE], fungal IE) or site of involvement (e.g., prosthetic valve endocarditis [PVE])

A

often classify IE based on the cause

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5
Q

subacute or acute

A

IE described as

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6
Q

with preexisting valve disease over a period of months.

A

subacute form affects those

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7
Q

those with healthy valves and appears as a rapidly progressive illness.

A

acute IE form affects

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8
Q

occurs when blood flow allows organisms to contact and infect previously damaged heart valves or other endothelial surfaces

A

Infective endocarditis pathophysiology

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9
Q

30% of cases are caused by Staphylococcus aureus.
- Other bacterial causes include Streptococcus viridans and coagulase-negative staphylococci.
-organisms make biofilms, which protect the organisms from immune defenses and make antimicrobials less effective

A

type of bacteria cause IF

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10
Q

used to be the most common cause of IE

A

Rheumatic heart disease (now less than 20%)

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11
Q

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

A

main risk factors for IE include

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12
Q

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

A

Common Risk Factors for Endocarditis

Cardiac Conditions

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13
Q

• Hospital-acquired bacteremia
• IV drug use

A

Common Risk Factors for Endocarditis

Noncardiac Conditions

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14
Q

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

A

Common Risk Factors for Endocarditis

Procedure-Associated Risks

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15
Q

(1) bacteremia,
(2) adhesion,
(3) vegetation.

A

IE typically develops in 3 stages:

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16
Q

, 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.

A

Vegetations, the primary lesions of IE

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17
Q

(e.g., brain, kidneys, spleen) and to the extremities, causing limb infarction

A

left-sided heart vegetation moves to various organs //emboli occurs with IE

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18
Q

, resulting in pulmonary emboli.

A

Right-sided heart lesions move to the lungs

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19
Q

dysrhythmias, valve dysfunction, and invasion of the myocardium, leading to heart failure (HF), sepsis, and heart block

A

infection may spread locally and damage the valves or their supporting structures. This causes

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20
Q

Most patients have fever.
- Fever may be low grade or may be absent in older adults or those who are immunocompromised. Other symptoms include chills, weakness, malaise, fatigue, and anorexia. Patients may have arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, and clubbing of fingers in subacute forms of IE

A

symptoms of IE

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21
Q

Vascular signs include splinter hemorrhages (black longitudinal streaks) in the nail beds. Petechiae from microembolization of vegetative lesions can occur on the conjunctivae, lips, buccal mucosa, and palate and over the ankles, feet, and antecubital and popliteal areas. Osler’s nodes (painful, tender, red or purple, pea-size lesions) are found on the fingertips or toes. Janeway’s lesions (flat, painless, small, red spots) may be seen on the fingertips, palms, soles of feet, and toes. Eye examination may show hemorrhagic retinal lesions called Roth’s spots.

A

symptoms of IE

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22
Q

new or worsening systolic murmur. Murmurs are usually absent in tricuspid IE because right-sided heart sounds are too low to be heard. HF is common, occurring in up to 80% of patients with aortic valve IE and 50% of those with mitral valve IE

A

IE symptoms and causes

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23
Q

is a potential complication of IE

A

Septic embolism

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24
Q

system, followed by extremities, spleen, and kidney.

A

central nervous system (CNS) is the most often affected organ from IE

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25
Q

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

A

health history to assess IE (Diagnostic study)

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26
Q

Three blood cultures drawn over a period of 1 hour from 3 different sites will be positive in most patients with IE

A

positive IE

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27
Q

is associated with antibiotic usage within the previous 2 weeks or results from a pathogen not easily detected by standard cultures A mild leukocytosis occurs in acute IE.

A

Culture-negative IE

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28
Q

erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels may be increased. Echocardiography can show vegetations.

A

Blood count shown to know IE indicated

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29
Q

on the Duke Criteria.

A

Guidelines for the diagnosis of IE are based

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30
Q

patient must have 2 major criteria and 1 minor criterion, or 1 major and 3 minor, or 5 minor criteria.

A

diagnosis of IE are based on Duke Criteria.

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31
Q

include positive blood cultures, typical microorganism for IE from 2 separate blood cultures, evidence of endocardial involvement, and new valvular vegetation.

A

Major criteria (diagnosis of IE based off Duke criteria)

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32
Q

predisposing (susceptible) heart condition or IV drug use, vascular phenomena, immunologic phenomena, microbiologic evidence, or echocardiographic findings consistent with IE but not meeting major criteria.

A

Minor criteria include (diagnosis of IE based off Duke criteria)

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33
Q

cardiomegaly (an enlarged heart).

A

chest x-ray may show

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34
Q

first- or second-degree atrioventricular (AV) block because the heart valves lie close to conductive tissue, especially the AV node.

A

An electrocardiogram (ECG) may show

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35
Q

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

A

people with the following heart conditions should receive prophylactic antibiotics

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36
Q

• 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
• Surgical procedures that involve infected skin, skin structures, or musculoskeletal tissue

A

When the target groups have the following conditions or procedures, they need prophylactic antibiotics:

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37
Q

every 24 to 48 hours until the infection is cleared.

A

Treatment -It is reasonable to obtain 2 sets of blood cultures

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38
Q

, an aortic root or myocardial abscess, or the wrong diagnosis (e.g., an infection elsewhere).

A

Cultures that stay positive indicate inadequate or inappropriate antibiotics

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39
Q

, follow-up echocardiogram and inflammatory (CRP) markers are done at 1, 3, 6, and 12 months.4

A

After completion of antibiotics

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40
Q

respond poorly to antibiotic therapy alone

A

Fungal IE and PVE (prosthetic valve endocarditis)

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41
Q

are for valve dysfunction leading to HF, to prevent embolization, or for uncontrolled infection.4

A

3 reasons to perform surgery

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42
Q

aspirin, acetaminophen, fluids, and rest.

A

Fever that persists after treatment has been started is managed with

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43
Q

the temperature stays elevated or there are signs of HF.
-IE with HF responds poorly to drug therapy and valve replacement, so it can be life threatening.

A

Complete bed rest is usually not needed unless

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44
Q

listen Murmur, Arthralgia (joint pain) and myalgias are common. 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. and emboli

A

Nursing Assessment

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45
Q

(1) normal or baseline heart function,
(2) ability to perform activities of daily living (ADLs) without fatigue, and (3) an understanding of the treatment plan to prevent recurrence.

A

overall goals for the patient with IE include

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46
Q

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 showing ischemia and conduction defects. Signs of systemic embolization or pulmonary embolism

A

possible diagnostic findings

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47
Q

Persistent temperature elevations may mean that the antibiotic is ineffective. Patients are at risk for life-threatening complications, such as stroke, pulmonary edema, and HF. Teach patients and caregivers to recognize signs and symptoms of these complications (e.g., change in mental status, dyspnea, chest pain, unexplained weight gain).

A

Teach pt and caregiver

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48
Q

adequate periods of physical and emotional rest. Bed rest may be needed when the patient has fever or complications (e.g., heart damage)

A

pt teaching if still has fever or complications

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49
Q

wear elastic compression stockings, perform ROM exercises, and deep breathe and cough every 2 hours.

A

pt treatment at home

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50
Q

Monitor laboratory data, including blood cultures, to determine antibiotic effectiveness. Assess IV lines for patency and signs of complications (e.g., phlebitis). Give antibiotics as prescribed. Monitor the patient for any adverse drug reactions.
Teach the patient and caregiver the nature of the disease and on how to reduce the risk for reinfection.
-Explain the relationship of follow-up care, good nutrition and dental care, and prompt treatment of common infections (e.g., colds) to stay healthy. Teach the patient about symptoms to report that may indicate another infection (e.g., fever, fatigue, chills). Finally, explain the importance of prophylactic antibiotic therapy before certain invasive procedures

A

Teach patient/ pt education

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51
Q

is a condition caused by inflammation of the pericardial sac (pericardium), often with fluid accumulation

A

Pericarditis

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52
Q

10 to 15 mL of serous fluid.

A

pericardial space between these 2 layers normally holds

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53
Q

inner serous membrane (visceral pericardium) and the outer fibrous (parietal) layer

A

pericardium is composed of the

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54
Q

anchors the heart, provides lubrication to decrease friction between heart contractions, and helps to prevent excess dilation of the heart during diastole.

A

pericardium function

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55
Q

is idiopathic (unknown) or viral

A

cause of acute pericarditis

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56
Q

acute, subacute, and chronic.

A

3 types of pericarditis:

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57
Q

develops rapidly, causing the pericardial sac to become inflamed and leak fluid (pericardial effusion).

A

Acute pericarditis

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58
Q

is inflammation. There is an influx of neutrophils, increased pericardial vascularity, and eventually fibrin deposition on the epicardium

A

characteristic pathologic finding in acute pericarditis

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59
Q

occurs weeks to months after an event.

A

Subacute pericarditis

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60
Q

pericarditis lasting more than 6 months aschronic.7

A

chronic pericarditis

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61
Q

Myocardial infarction (MI) causes 5% to 8% of acute pericarditis cases

A

causes of acute pericarditis

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62
Q

can occur 4 to 6 weeks after transmural MI . This syndrome is more common after a large anterior infarct.

A

Post-MI syndrome (Dressler syndrome) pericarditis

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63
Q

is often seen after respiratory or GI illness.

A

Viral pericarditis

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64
Q

severe, sharp chest pain.
-The pain is generally worse with deep inspiration and when lying flat. Sitting up and leaning forward relieves the pain.
-The pain may radiate to the neck, arms, or left shoulder, making it hard to distinguish from angina. One distinction is that the pain from pericarditis can be referred to the trapezius muscle (shoulder, upper back).
-Dyspnea is related to the patient’s breathing in rapid, shallow breaths to avoid chest pain. Fever and anxiety may worsen dyspnea.

A

signs and symptoms of pericarditis

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65
Q

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

A

common causes of pericarditis / infectious

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66
Q

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

A

common causes of pericarditis / non-infectious

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67
Q

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

A

common causes of pericarditis / Hypersensitive or Autoimmune

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68
Q

in acute pericarditis is 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.

A

The hallmark finding of pericarditis

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69
Q

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

A

hearing pericarditis

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70
Q

, ask the patient to hold their breath. If you still hear the rub, it is cardiac

A

pericardial friction rub from a pleural friction rub

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71
Q

are pericardial effusion and cardiac tamponade.

A

major complications of pericarditis

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72
Q

is a build-up of fluid in the pericardium. It can occur rapidly (e.g., chest trauma) or slowly (e.g., tuberculosis pericarditis).

A

Pericardial effusion

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73
Q

Large effusions compress nearby structures.
- Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. Phrenic nerve compression can cause hiccups. Compression of the laryngeal nerve may result in hoarseness. Heart sounds are generally distant and muffled. BP is usually maintained.

A

Sign and symptoms of pericardial effusion

74
Q

develops as the pericardial effusion volume increases and compresses the heart.

A

Cardiac tamponade

75
Q

acutely (e.g., rupture of heart, trauma) or subacutely (e.g., from renal failure, cancer).

A

Cardiac tamponade can occur

76
Q

chest pain and is often confused, anxious, and restless. As the compression of the heart increases, there is decreased CO, muffled heart sounds, narrowed pulse pressure, tachypnea, and tachycardia. Neck veins are markedly distended because of increased jugular venous pressure. Pulsus paradoxus, if present, is a large decrease in systolic BP during inspiration . In a patient with a slow onset of a cardiac tamponade, dyspnea may be the only manifestation.

A

cardiac tamponade sign and symptoms

77
Q

ECG is useful in diagnosing acute pericarditis, with changes noted in 90% of cases. The most sensitive ECG changes include diffuse (widespread) ST segment elevations. This reflects the abnormal repolarization from the pericardial inflammation. These changes are different from the ST changes seen in MI. In myocardial ischemia, there are usually localized ST segment changes. In acute pericarditis serial ECGs do not show evolving changes,

A

Pericarditis Diagnostic studies/ labs

78
Q

Doppler imaging and color M-mode can assess diastolic function and diagnose constrictive pericarditis (discussed later in the chapter). A CT scan and MRI can visualize the pericardium and pericardial space.
-Common laboratory findings include leukocytosis and increased CRP and ESR. Troponin levels may be increased in patients with ST segment elevation and acute pericarditis, which could indicate concurrent heart damage. Fluid obtained during pericardiocentesis or tissue from a pericardial biopsy may be studied to determine the cause of the pericarditis.

A

pericarditis diagnosis

79
Q

Chest x-ray findings are generally normal, but a large pericardial effusion may appear as cardiomegaly

A

pericardial effusion diagnostic

80
Q

echocardiogram can determine the presence of a pericardial effusion or cardiac tamponade

A

cardiac tamponade diagnostics

81
Q

Antibiotics treat bacterial pericarditis, and nonsteroidal antiinflammatory drugs (NSAIDs) (e.g., salicylates [aspirin], ibuprofen) control the pain and inflammation

A

pericarditis treatment

82
Q

Corticosteroids are used for patients with pericarditis from systemic lupus erythematosus, patients already taking corticosteroids for autoimmune conditions, or patients who do not respond to NSAIDs
-Colchicine, an antiinflammatory drug used for gout, may help patients who have recurrent pericarditis

A

pericarditis treatment

83
Q

is usually done for pericardial effusion with acute cardiac tamponade, purulent pericarditis, or suspected cancer. Hemodynamic support for the patient before the procedure may include giving volume expanders and inotropic agents (e.g., dopamine) and stopping any anticoagulants. The procedure is done rapidly and safely using a percutaneous approach guided by echocardiography

A

Pericardiocentesis

84
Q

is a surgical procedure for diagnosis or drainage of excess fluid. Cutting a “window,” or part of the pericardium, allows the fluid to drain continuously into the peritoneum or chest.

A

pericardial window

85
Q

• History and physical examination (assess for pericardial friction rub, pulsus paradoxus)
• Laboratory: CRP, ESR, white blood cell count
• ECG
• Chest x-ray
• Echocardiogram
• CT scan
• MRI
• Pericardiocentesis, pericardial window
• Pericardial biopsy

A

acute pericarditisis Diagnostic assessment

86
Q

• Treatment of underlying disease
• Bed rest
• Drug therapy
• NSAIDs
• Corticosteroids
• Pericardiocentesis (for tamponade)
• Pericardial window (for tamponade or ongoing pericardial effusion)
CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.

A

Management pericarditis

87
Q

results from fibrotic thickening and rigidity of the pericardium, usually after an episode of acute pericarditis

A

Chronic constrictive pericarditis

88
Q

It is characterized by fibrin deposition and pericardial effusion. Reabsorption of the effusion slowly follows, with progression to fibrous scarring, thickening of the pericardium from calcium deposits, and eventual destruction of the pericardial space. The fibrotic, thickened, and adherent pericardium encases the heart and prevents adequate atrial and ventricular stretch.

A

pathophysiology of chronic constrictive pericarditis

89
Q

mimic HF and cor pulmonale. Decreased CO accounts for many of the manifestations. These include dyspnea on exertion, peripheral edema, ascites, fatigue, anorexia, and weight loss. The most prominent finding on physical examination is jugular venous distention (JVD). Unlike with cardiac tamponade, the presence of pulsus paradoxus (greater than 10 mm Hg) is not common.6

A

signs and symptoms chronic constrictive pericarditis

90
Q

ECG changes are often nonspecific in chronic constrictive pericarditis. The heart on the chest x-ray may be normal or enlarged. Echocardiography findings may show a thickened pericardium but without a large pericardial effusion. CT and MRI can measure pericardial thickness and assess diastolic filling patterns.

A

Diagnostic studies for chronic constrictive pericarditis

91
Q

pericardiectomy. This involves complete resection of the pericardium through a median sternotomy with the use of cardiopulmonary bypass. Some patients show immediate improvement, but others may take weeks. The prognosis improves when the patient has surgery before becoming clinically unstable.

A

Treatment for chronic constrictive pericarditis

92
Q

is a focal or diffuse inflammation of the myocardium.

A

Myocarditis

93
Q

Causes include viruses, bacteria, fungi, radiation therapy, and pharmacologic and chemical factors. Coxsackie A and B viruses are the most common causative agents. Autoimmune disorders (e.g., polymyositis) have been linked with the development of myocarditis. It also may be idiopathic.

A

Myocarditis causes

94
Q

, the causative agent invades the myocytes and causes cellular damage and necrosis. This activates the immune response. Cytokines and O2 free radicals are released. As the infection progresses, an autoimmune response is activated. This causes further destruction of myocytes. Myocarditis results in heart dysfunction. Dilated cardiomyopathy can occur

A

myocardium becomes infected pathophysiology

95
Q

benign course without any overt symptoms to progressive HF, dysrhythmias, or sudden cardiac death (SCD).8 Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and nausea and vomiting are early manifestations of the viral illness.
Early cardiac signs appear 7 to 10 days after viral infection because pericarditis often accompanies myocarditis. These include pleuritic chest pain with a pericardial friction rub and effusion.

A

signs and symptoms of myocarditis

96
Q

Late cardiac signs relate to the development of HF and include an S3 heart sound, crackles, JVD, syncope, peripheral edema, and angina.

A

late myocarditis sign and symp

97
Q

CG changes with myocarditis are often nonspecific but reflect associated pericardial involvement (e.g., diffuse ST segment changes). Dysrhythmias and conduction problems may be present. Laboratory findings are often inconclusive. They may include mild to moderate leukocytosis and atypical lymphocytes, elevated viral titers, and increased ESR, CRP levels, and levels of cardiac biomarkers, such as troponin. The virus is generally present in tissue and pericardial fluid samples only during the first 8 to 10 days of illness.
Endomyocardial biopsy provides histologic confirmation of myocarditis.
A biopsy is most diagnostic during the first 6 weeks of acute illness, when lymphocytic infiltration and myocyte damage are present. Nuclear scans, echocardiography, and MRI are used to assess heart function.

A

diagnostic studies in myocarditis

98
Q

Angiotensin-converting enzyme (ACE) inhibitors and β-adrenergic receptor blockers (β-blockers) are used if the heart is enlarged or to treat HF (see Chapter 34). Diuretics reduce fluid volume and preload. If the patient is not hypotensive, IV drugs such as nitroprusside and milrinone reduce afterload and improve CO by decreasing systemic vascular resistance. Digoxin (Lanoxin) improves heart contractility and reduces HR. It is used cautiously in patients with myocarditis because of increased sensitivity to the adverse effects (e.g., dysrhythmias) and the potential toxicity. Anticoagulation reduces the risk for clot formation from blood stasis in patients with a low ejection fraction (EF).

A

treatment for myocarditis

99
Q

immunosuppressive agents.
-However, the use of these drugs for the treatment of myocarditis is controversial because they may lead to recurrence.8 In some instances, antivirals may be used as adjunct therapy to treat myocarditis.

A

Myocarditis with an autoimmune basis is treated with

100
Q

General supportive measures include O2 therapy, bed rest, and restricted activity. In cases of severe HF, intraaortic balloon pump therapy and ventricular assist devices (VAD) may be needed

A

nursing considerations myocarditis

101
Q

is an acute inflammatory disease that can involve all the heart layers. RF occurs most often between the ages of 5 and 15.9Rheumatic heart disease is a chronic scarring and deformity of the heart valves resulting from RF.

A

Rheumatic fever (RF)

102
Q

RF occurs as a complication 2-3 weeks after a group A streptococcal pharyngitis. Signs of RF appear to be from an abnormal immune response to bacterial antigens.9 RF affects the heart, skin, joints, and CNS. Rheumatic heart disease, caused by RF, primarily affects young adults.
RF has declined in developed countries because of the effective use of antibiotics to treat streptococcal infections. However, it is an important public health problem in developing countries.9 Risk factors include age, gender, and environmental factors.1

A

Rheumatic fever and heart disease pathophysiology

103
Q

About 50% of RF episodes are rheumatic pancarditis, involving all layers of the heart (endocardium, myocardium, and pericardium)

A

RF affects

104
Q

, with swelling and erosion of the valve leaflets. Vegetation forms from deposits of fibrin and blood cells in areas of erosion. The lesions initially create thickening of the valve leaflets, fusion of commissures and chordae tendineae, and fibrosis of the papillary muscle. Valve leaflets may become calcified, resulting in stenosis

A

Rheumatic IE is found mainly in the valves

105
Q

are formed by a reaction to inflammation with swelling and destruction of collagen fibers.

A

Nodules, called Aschoff’s bodies,

106
Q

Nodules, called Aschoff’s bodies, are formed by a reaction to inflammation with swelling and destruction of collagen fibers. As the Aschoff’s bodies age, they become more fibrous, and scar tissue forms in the myocardium.
develops and affects both layers of the pericardium.

A

Rheumatic pericarditis

107
Q

layers become thick and covered with a fibrinous exudate.

A

erosanguineous pericardial effusion may develop

108
Q

systemic lesions of RF involve the skin, joints, and CNS. Painless subcutaneous nodules, arthralgias or arthritis, and chorea may develop.

A

Extracardiac lesions develop from RF

109
Q

uses swelling, heat, redness, tenderness, and limitation of motion.
-arger joints, particularly the knees, ankles, elbows, and wrists, are most often affected.

A

Monoarthritis or polyarthritis manifestation of RF.

110
Q

3 signs: (1) heart murmur or murmurs of mitral or aortic regurgitation, or mitral stenosis; (2) heart enlargement and HF from myocarditis; and (3) pericarditis resulting in muffled heart sounds, chest pain, pericardial friction rub, or signs of effusion.

A

Carditis is the most important manifestation of RF.

111
Q

is the major CNS manifestation.9 It is characterized by involuntary movements, especially of the face and limbs; muscle weakness; and speech and gait problems.

A

Sydenham’s chorea (manifestation of RF.)

112
Q

bright pink, nonpruritic, maplike macular lesions occur mainly on the trunk and proximal extremities. They intensify with heat (e.g., warm bath).

A

Erythema marginatum lesions are a less common feature of RF

113
Q

associated with severe carditis are small, hard, painless swellings found over extensor surfaces of joints, particularly the knees, wrists, and elbows.

A

Subcutaneous nodules feature of RF

114
Q

No single diagnostic test exists for RF. An echocardiogram may show valvular insufficiency and pericardial fluid or thickening.11 A chest x-ray may show an enlarged heart. The most consistent ECG change is a prolonged PR interval from delayed AV conduction.

A

diagnostic of RF

115
Q

drug therapy and supportive measures. Antibiotic therapy does not change the course of the acute disease or the development of carditis. It eliminates residual group A streptococci in the tonsils and pharynx and prevents the spread of organisms to close contacts. Salicylates, NSAIDs, and corticosteroids are the antiinflammatory agents most widely used to control the fever and joint manifestations.

A

RF Treatment consists of

116
Q

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) need lifelong prophylaxis

A

Treatment Patients with RF without carditis

117
Q

(mitral and tricuspid) and 2 semilunar valves (aortic and pulmonic) control blood flow through the heart

A

Two AV valves

118
Q

the valves affected and the type of dysfunction: stenosis or regurgitation

A

Valvular heart disease is defined by

119
Q

, the valve opening is smaller. The forward flow of blood is impaired. This creates a difference in pressure on the 2 sides of the open valve.

A

stenotic valve

120
Q

(i.e., the higher the difference, the greater the stenosis)

A

amount of stenosis (constriction or narrowing) is seen in the pressure differences

121
Q

, there is incomplete closure of the valve. This results in the backward flow of blood.

A

regurgitation occurs (referred to as incompetence or insufficiency)

122
Q

in children and adolescents

A

Congenital heart conditions are the most common cause of valve disorders

123
Q

older adults who have some form of heart disease. Other causes of valve disease in adults are related to acquired immunodeficiency syndrome and the use of some antiparkinsonian drugs.12

A

RISK Aortic stenosis and mitral regurgitation (MR) often occur in

124
Q

is rheumatic heart disease

A

most common cause of mitral stenosis

125
Q

deformities block the blood flow and create a pressure difference between the left atrium and left ventricle during diastole. As a result, left atrial pressure and volume increase, causing higher pulmonary vasculature pressure. The overloaded left atrium places the patient at risk for atrial fibrillation. In chronic mitral stenosis, pressure overload occurs in the left atrium, pulmonary bed, and right ventricle

A

mitral stenosis pathophysiology

126
Q

is exertional dyspnea caused by reduced lung compliance . Heart sounds include a loud first heart sound and a low-pitched, diastolic murmur (best heard at the apex with the stethoscope). Less often, patients may have hoarseness (from atrial enlargement pressing on the laryngeal nerve), hemoptysis (from pulmonary hypertension), and chest pain (from decreased CO and coronary perfusion). Emboli can form in the left atrium from atrial fibrillation and cause a stroke

A

main symptom of mitral stenosis

127
Q

intact mitral leaflets, mitral annulus, chordae tendineae, papillary muscles, left atrium, and left ventricle

A

Mitral valve function depends on

128
Q

defect in any of these structures can cause regurgitation. MR may result from problems with the leaflets or from the surrounding structures. I

A

Mitral valve cause of dysfunction

129
Q

, a problem with the leaflets causes the regurgitation.

A

In primary (degenerative) MR

130
Q

, myocardial disease causes the regurgitation. Most cases of MR are caused by MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and IE.

A

In secondary (functional) MR

131
Q

, the added volume results in left atrial enlargement, left ventricular dilation and hypertrophy, and, finally, a decrease in CO.

A

chronic MR

132
Q

may remain asymptomatic for many years. Early symptoms of left ventricular failure may include weakness, fatigue, palpitations, and dyspnea. These gradually progress to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema. Increased left ventricular volume leads to an audible third heart sound (S3), even with normal left ventricular function. The murmur is a loud holosystolic murmur at the apex radiating to the left axilla.

A

chronic MR

133
Q

typically requires valve repair or replacement before significant left ventricular failure or pulmonary hypertension develop.

A

treatment Primary MR

134
Q

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

A

Mitral valve prolapse (MVP)

135
Q

can be misleading because it is used even when the valve is working normally.

A

prolapse

136
Q

, but serious complications can occur, including MR, IE, SCD, HF, and cerebral ischemia.

A

MVP is usually benign

137
Q

there is an increased familial incidence. The genetic inheritance is often autosomal dominant

A

MVP is unknown,

138
Q

a connective tissue defect affecting only the valve, or as part of Marfan’s syndrome or other hereditary conditions that affect collagen structure

A

MVP in this group results from

139
Q

is a regurgitation murmur that is louder during systole

A

MVP

140
Q

M-mode and 2-D echocardiography are used to confirm MVP

A

diagnosis studies used for MVP

141
Q

β-Blockers may control palpitations and chest pain. Encourage the patient to stay hydrated, exercise regularly, and avoid caffeine.

A

treatment MVP (don’t use nitro)

142
Q

is generally found in childhood, adolescence, or young adulthood. In older adults, AS is a result of RF or degeneration, similar to coronary artery disease.

A

Congenital aortic stenosis (AS)

143
Q

rheumatic valve disease, fusion and calcification cause the valve leaflets to stiffen and retract, resulting in

A

stenosis pathiophsiology

144
Q

may be the result of primary disease of the aortic valve leaflets, the aortic root, or both.
- Trauma, IE, or aortic dissection can cause acute AR,

A

Aortic regurgitation (AR)

145
Q

generally results from rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, a connective tissue problem, or a postsurgical cause.19

A

Chronic AR causes

146
Q

This results in volume overload. The left ventricle initially compensates for chronic AR by dilation and hypertrophy. Myocardial contractility eventually declines, and blood volume in the left atrium and pulmonary bed increases. This leads to pulmonary hypertension and right ventricular failure.

A

AR causes retrograde (backward) blood flow from the ascending aorta into the left ventricle during diastole.

147
Q

sudden signs of cardiovascular collapse (Table 36.10). The patient develops severe dyspnea, chest pain, and hypotension indicating left ventricular failure and cardiogenic shock, a life-threatening emergency.

A

acute AR have

148
Q

can be primary or secondary

A

Tricuspid regurgitation (TR)

149
Q

is less common and is typically due to IE.

A

Primary TR

150
Q

right ventricular (RV) dilatation from pulmonary hypertension, cor pulmonale, or pulmonary outflow tract obstruction. The patient does not show JVD, enlarged liver, and peripheral edema until regurgitation is severe

A

Secondary TR is caused by

151
Q

is almost always caused by RF

A

Tricuspid stenosis

152
Q

is almost always a congenital part of TOF. It results in right ventricular hypertension and hypertrophy . It is largely asymptomatic. When symptoms develop, they are similar to those of AS (syncope, dyspnea, angina). Symptoms typically do not present until adulthood.

A

Pulmonic stenosis

153
Q

echocardiogram shows valve structure, function, and heart chamber size. Transesophageal echocardiography and Doppler color-flow imaging help diagnose and monitor valvular heart disease progression. Real-time 3-D echocardiography can help assess mitral valve and congenital heart disease.

A

valvular heart disease (Diagnostic studies)

154
Q

• Vasodilators∗ (e.g., nitrates, ACE inhibitors)
• Positive inotropes (e.g., digoxin)
• Diuretics
• β-Blockers

A

Drug therapy to treat or control HF

155
Q

Atrial dysrhythmias are common. They are treated with calcium channel blockers, β-blockers, antidysrhythmic drugs, or electrical cardioversion

A

Atrial dysrhythmias /a.fib

156
Q

alternative treatment for some patients with valvular heart disease is

A

percutaneous transluminal balloon valvuloplasty (PTBV)

157
Q

Balloon valvuloplasty treats mitral, tricuspid, pulmonic, and AS.

A

Balloon valvuloplasty treatment

158
Q

It involves threading a balloon-tipped catheter from the femoral artery or vein to the stenotic valve. The balloon is inflated to separate the valve leaflets. A single- or double-balloon technique may be used. Using a single Inoue balloon with hourglass shape allows sequential inflation. This technique is the most popular because it is easy and has good results with few complications

A

Balloon valvuloplasty

159
Q

The THV is inserted through the femoral artery and moved to the heart. It is released and expanded with a balloon in the location of the aortic valve. This procedure is limited to patients who are eligible for surgery but who are at high risk for surgical complications (e.g., those with multiple co-morbidities).

A

Sapien Transcatheter Heart Valve (THV) is used for select patients with AS.

160
Q

often used in mitral or tricuspid valve disease.

A

valve repair

161
Q

involves repair of the valve by suturing the torn leaflets, chordae tendineae, or papillary muscles. It is primarily used to treat mitral or tricuspid regurgitation.

A

Open surgical valvuloplasty

162
Q

mitral or tricuspid regurgitation, further valve repair or reconstruction using annuloplasty is an option. Annuloplasty involves reconstruction of the annulus, with or without the aid of prosthetic rings.

A

Annuloplasty

163
Q

wide variety of prosthetic valves are available. Desirable valves are nonthrombogenic, are durable, and create minimal stenosis.

A

Valve replacement

164
Q

Valves are either mechanical or biologic (tissue) valves

A

2 types of valve replacement

165
Q

are made from artificial materials. They consist of combinations of metal alloys, pyrolytic carbon, and Dacron.

A

Mechanical valves

166
Q

are made from bovine, porcine, and human (cadaver) heart tissue. They usually contain some human-made materials
-produce a more natural pattern of blood flow compared with mechanical valves.

A

Biologic valves

167
Q

are more durable and last longer than biologic valves. However, they have an increased risk for thromboembolism. Patients need long-term anticoagulation therapy, which increases the risk of bleeding.13

A

Mechanical valves vs biologic valves

168
Q

they are less durable and tend to cause early calcification, tissue degeneration, and stiffening of the leaflets

A

biologic valves

169
Q

are another option for treating valvular heart disease. They are used to treat patients at high risk for surgery who have aortic or mitral bioprosthetic valve failure.

A

Transcatheter therapies

170
Q

is approved for use in pediatric and adult patients with pulmonary valve disease caused by congenital heart disease.

A

Transcatheter pulmonary valve replacement

171
Q

is an option for patients with severe, symptomatic AS who are at intermediate risk or higher for surgical aortic valve replacement (SAVR)
-transfemoral approach.

A

Transcatheter aortic valve replacement (TAVR)

172
Q

echocardiogram, coronary CT angiogram, heart catheterization, and pulmonary function testing.21 Imaging can determine valve size and plan the procedure.

A

evaluation for TAVR includes

173
Q

in the United States

A

2 TAVR valves

174
Q

is made of bovine pericardial tissue. It is a balloon expandable valve

A

Edwards Sapien 3 valve (1 of 2 types of TAVR valve)

175
Q

is a group of diseases that directly affect myocardial structure or function

A

Cardiomyopathy (CMP)

176
Q

as primary or secondary

A

Cardiomyopathy (CMP) classified

177
Q

refers to those conditions in which the cause is idiopathic. The heart muscle is the only part of the heart involved, and other heart structures are unaffected

A

Primary CMP

178
Q

, the cause of the myocardial disease is known and is due to another disease process

A

secondary CMP

179
Q

are dilated, hypertrophic, and restrictive

A

3 major types of CMP

180
Q

CMP that leads to cardiomegaly and HF is the

A

main reason for heart transplants CMP

181
Q

is a transient heart syndrome that mimics acute coronary syndrome

A

Takotsubo cardiomyopathy-more common in postmenopausal woman

182
Q

Patients often have chest pain, ST segment elevation on ECG, and elevated cardiac biomarkers consistent with an MI

A

diagnostics Cardiomyopathy

adn semester 2 (19 decks)

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