Inflammatory/ Structural Heart Disorder- Ch 37

Question 0

Classification of infective endocarditis

Answer 0

1. Subacute: affects those with preexisting valve disease and has clinical course that may extend over month
2. Acute : affect those have a healthy valves and manifest as a rapid progressive illness

Question 1

Definition Infective endocarditis

Answer 1

Indection of the endocardial layer of the heart, due to bacteria and fungi

Causative agent: staphylococcus aureus and streptococcus viridans

Question 2

Etiology of ineffective endocarditis

causative agent

Answer 2

The most common causative organism of Infective endocarditis:
Staphylococcus aureus
Streptococcus viridans

Other possible pathogen include fungi and viruses

Question 3

Vegetation

Answer 3

The primary lesions of infective endocarditis, consist of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium

Loss of part of these fragile vegetation can cause emboli
+ from left side heart: vegetation move to various organs (brain, kidney, liver), and to the extremities cause limb infarction
+ from right side heart: move to the lung, cause pulmonary emboli.

Question 4

The main contributing factors to Infective endocarditis

Answer 4

Aging
IVDA
Use of prosthetic valves
Use of intravascular devices resulting health- care associated infections
Renal dialysis

Question 5

Clinical manifestation of Infective endocarditis

Answer 5

Low grade fever
Chill, weakness, malaise, fatigue, and anorexia

In subacute form of endocarditis: arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, clubbing of the finger.

Splinter hemorrhages ( black longitudinal streaks)
Petechiae ( occur in conjunctivae, lips, buccal mucosa, palate, and over ankle, feet, and antecubital, and popliteal area.

Osler’s nodes ( painful, tender, red or purple, pea-size lesions

Question 6

Diagnosis of infective emdocarditis

Answer 6

Positive blood culture
New or changed heart murmur
Intracardiac mass or vegetation noted on echocardiography

Question 7

Collaborative care of infective endocarditis

Answer 7

IV antibiotic therapy
Fungal endocarditis and PVE respond poorly to antibiotic alone, thus early valve replacement along with 6 weeks antibiotic is recommended.
Treat fever with aspirin, acetaminophen (Tylenol), ibuprofen, fluids, and rest.

Question 8

Nursing management of Infective cardititis

Answer 8

1. Assessment: VS and heart sound to detect a murmur
   Arthralgia may involve multiple joints, thus assess for joint tenderness, decreased ROM, muscle tenderness
   Examine for petechiae, splinter, hemorrhages, and osler’s nodes.
2. Nursing implementation
   + patient teaching about disease, hygiene, prevention of infection, avoid excessive fatigue, antibiotic adherence
   + teach the patient the signs and symptoms of complications.
   + follow up care, good nutrition, early treatment.

Question 9

Acute pericarditis

Answer 9

Pericarditis is a condition causes by inflammation of the pericardial sac (the pericardium)
The pericardium: serous membrane ( visceral pericardium) and the outer fibrous (parietal ) layer.

Question 10

Etiology and pathophysiology of pericarditis

Answer 10

Most often, the causes of pericarditis is idiopathic ( unknown), with a variety of suspected viral cause. The coxsackie B virus is the most common identified virus.

Pericaridits with MI: acute pericarditis (48-72 hr after an MI), and Dressler Syndrome ( late pericarditis, 4-6 weekd after MI)

Question 11

Clinical manifestation of pericarditis

Answer 11

Progressive, frequent, sharp chest pain ( the pain is worse with deep inspiration, and when lying supine)
Pain may radiate to neck, arm, left shoulder
Pain from trapezius muscle( shoulder, upper back) since the phrenic nerve innervation
Dyspnea ( rapid, shallow breath) to avoid chest pain and may be aggravated by fever, and anxiety.
Pericardial fiction rub- a scratching, grating, high-pitched sound result from friction between the roughed pericardial and epicardial surfaces (easier to hear with pt hold his breath).

Question 12

Pericardial effusion

Answer 12

Build up of fluid in the pericardium
Large effusion my compress nearby structures. Pulmonary compression can cause cough, dyspnea, and tachypnea.heart sounds are generally distant and muffed, although blood pressure usually is limited.

Question 13

Cardiac tamponade

Answer 13

Cardiac tamponade may develop as the pericardial effusion increase in volume, resulting compression of the heart.
Patient with cardiac tamponade may report chest pain, confused, anxious, and restless. As the compression of the heart increase, decreased CO, muffled heart sounds, and narrowed pulse pressure.
Neck vein distended
Pulse paradoxus ( decrease in systolic BP during inspiration)
Dyspnea may only the clinical manifestation with slow onset

Question 14

Diagnostic of acute pericarditis

Answer 14

History and physical examination : pericardial
 friction rub, pulsus paradoxus
Laboratory: CRP, ESR, white blood cell count
Electrocardiogram
Chest X-ray
Echocardiogram
Computed tomography
Magnetic resonance imaging
Pericardiocentesis, pericardial window
Pericardial biopsy

Question 15

Collaborative care of acute pericardotis

Answer 15

Treatment of underlying disease
Be rest
Nonsteroidal antiinflammatory drugs ( nSAIDS) - salicylates, ibuprofen,..
Corticosteroids
Pericardiocentesis ( for tamponade)
Pericardial window ( for tamponade or ongoing pericardial effusion)

Question 16

Pericardiocentesis

Answer 16

pericardiocentesis is a procedure where fluid is aspirated from the pericardium (the sac enveloping the heart).
Pericardiocentesis is usually performed for pericardial effusion with acute cardiac tamponade, purulent pericarditis

Hemodynamic support: administer of volume expander, and inotropic agent ( e.g Intropin) and the discontinuation of any anticoagulation

A needle is inserted into the pericardial space to remive fluid for analysis and to relieve cardiac pressure

Complication of pericardiocentesis: dysrhythmias, further cardiac tamponade, pneumomediastinum, pneumohorax, myoxardial laceration, and coronary artery laceration.

Question 17

Pericardial window

Answer 17

Used to diagnosis and for drainage of excess fluid.

Cutting a window” or a portion of the pericardium. This allow fluid to drain continuously into the peritoneum or chest.

Question 18

Nursing management if acute pericarditis

Answer 18

Distinguish pain of angina from the pajn of pericarditis . Pericarditis pain: located at the precordium or left trapezius region, has sharp, pleuritic quality that increase with inspiration. Pakn is often relieved when the patient sit up or lean forward, and is worse when lying supine

+ ECH: in acute pericarditis, there are diffuse ST segment elevation. In myocardial ischemia, there are usually localized ST segment changes.

• • pain relief: high fowler 45 degree, over bed table for support, antiinflammatory medications ( administer these drugs with food or milk, avoid alcohol).
• • anxiety reduce, provide information
• • monitor signs of cardiac tamponade, prepare for possible pericardiocentesis

Question 19

Valvular heart disease types: stenosis and regurgitation

Answer 19

Stenosis: constriction or narrowing- is seen in the pressure differences ( the higher the difference, the greater the stenosis)

Regurgitation: (incompetence or insufficiency), incomplete closure of the valve results in the backward flow of blood

Question 20

Mitral valve stenosis

Answer 20

Most cases of mitral valves stenosis result from rheumatic heart disease

Rheumatic endocarditis causes scarring of the valve leaflets and the chordae tendineae –> contractures and adhesions develop between the commissures –> thickening and shortening of the mitral valves structures –> “fish mouth” shape stenosed valve –> block the flow and create a pressure difference between the left atrium and the left ventricle during diastole –> higher pulmonary vascular pressure –> risk for atrial fibrillation

Question 21

Clinical manifestation of mitral valve stenosis

Answer 21

Exertional dyspnea (due to reduced lung compliance)
Loud, ascentuated S1; low-pitched, diastolic murmur
Hoarseness (from atrial enlargement pressing on the laryngeal nerve)
Hemoptysis ( from pulmonary hypertension)
Chest pain ( from decreased CO and coronary perfusion)
Seizures or stroke (from emboli)
Fatigue and palpitations from atrial fibrillation
Emboli can arise from blood stasis in the left atrium secondary to atrial fibrillation

Question 22

Mitral valve regurgitation

Answer 22

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

Question 23

Aortic valve stenosis

Answer 23

In rheumatic valve disease, fusion of the commissures and secondary calcification cause the valve leaflets to stiffen and retract, resulting stenosis.

Aortic stenosis causes obstruction of flow fron the left ventricle to the aorta during systole –> left ventricle hypertrophy and increased myocardial consumption –> reduced CO–> decreased tissue perfusion, pulmonary hypertension, and HF

Question 25

Clinical manifestation of aortic stenosis

Answer 25

Valve orifice becomes about one third its normal size
Classic triad of angina, syncope, and exertional dyspnea ( left ventricle failure)
SAD
Normal or soft S1, diminished or absent S2, systolic murmur, prominent S4

Nitroglycerin is used cautiously to treat angina, since the drug can significantly reduce blood pressure and worsen chest pain.

Question 26

Diagnostic study for valvular heart disease

Answer 26

+ History and physical examination
+ chest X-ray: reveal heart size, altered pulmonary circulation, and valve calcification.
CBC
+ Electrocardiogram: reveal valve structure, function, and heart chamber size.
+ Echocardiography (dropler and transesophageal)
+ cardiac catherization: detects pressuer changes in the cardiac chambers, records pressuer differences across the valves, and measures the size of valve opening

Question 27

Collaborative care of valvular heart disease

Answer 27

Nonsurgical and surgical

Question 28

Nonsurgical -collaborative care of valvular heart disease

Answer 28

\+ prophylactic antibiotic therapy: 
         - rheumatic fever
        - infective endocarditis
\+ sodium restriction
\+medication to treat or control heart failure
       - vasodilators (nitrates, ACE inhibitors)
      - positive inotropes ( digoxin)
      - diuretics
      - Beta -adrenergic blockers
\+ Anticoagulation therapy
\+ antidysrhythmias drugs
\+ pecutaneous transluminal balloon valvuloplasty
\+ percutaneous valve replacement

Question 29

Surgical therapy for valvular heart disease

Answer 29

1. Valve repair:
   a. commissurotomy (valvutomy): treat pure mitral stenosis.
   - In closed procedure, the surgeon insert a tranventricular dilator through the apex of the left ventricle into the opening of the mitral valve.
   - open procedure: require the use of cardiopulmonary bypass. Remove thrombi from the atrium, and make a commissure incision, then the fused chordae are separated by splinting the papilary muscle and debriding the calcified valve.
   b. valvuloplasty
   + open surgical valculoplasty: repair the valve by suturing the torn leaflets, chordae tendinae, or papillary muscles –> to treat mitral or tricupsid regurgitation
   + minimally invasive valvuloplasty: ministernotomy and parasternal approach. shorter length of stay, fewer blood transfusion, less pain, and lower risk of sternal infection and postoperative atrial fibrillation.
   c. annuloplasty: reconstruction of the ann