Inflammatory/ Structural Heart Disorder- Ch 37 Flashcards
Classification of infective endocarditis
- Subacute: affects those with preexisting valve disease and has clinical course that may extend over month
- Acute : affect those have a healthy valves and manifest as a rapid progressive illness
Definition Infective endocarditis
Indection of the endocardial layer of the heart, due to bacteria and fungi
Causative agent: staphylococcus aureus and streptococcus viridans
Etiology of ineffective endocarditis
causative agent
The most common causative organism of Infective endocarditis:
Staphylococcus aureus
Streptococcus viridans
Other possible pathogen include fungi and viruses
Vegetation
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.
The main contributing factors to Infective endocarditis
Aging IVDA Use of prosthetic valves Use of intravascular devices resulting health- care associated infections Renal dialysis
Clinical manifestation of Infective endocarditis
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
Diagnosis of infective emdocarditis
Positive blood culture
New or changed heart murmur
Intracardiac mass or vegetation noted on echocardiography
Collaborative care of infective endocarditis
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.
Nursing management of Infective cardititis
- 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. - 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.
Acute pericarditis
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.
Etiology and pathophysiology of pericarditis
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)
Clinical manifestation of pericarditis
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).
Pericardial effusion
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.
Cardiac tamponade
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
Diagnostic of acute pericarditis
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
Collaborative care of acute pericardotis
Treatment of underlying disease
Be rest
Nonsteroidal antiinflammatory drugs ( nSAIDS) - salicylates, ibuprofen,..
Corticosteroids
Pericardiocentesis ( for tamponade)
Pericardial window ( for tamponade or ongoing pericardial effusion)
Pericardiocentesis
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.
Pericardial window
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.
Nursing management if acute pericarditis
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
Valvular heart disease types: stenosis and regurgitation
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
Mitral valve stenosis
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
Clinical manifestation of mitral valve stenosis
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
Mitral valve regurgitation
Most cases of mitral regurgitation are caused by MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and IE
Aortic valve stenosis
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
Clinical manifestation of aortic stenosis
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.
Diagnostic study for valvular heart disease
+ 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
Collaborative care of valvular heart disease
Nonsurgical and surgical
Nonsurgical -collaborative care of valvular heart disease
\+ 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 replacementSurgical therapy for valvular heart disease
- 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
