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Inflammatory and Valvular Heart Diseases
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Rheumatic Fever and Heart Disease
Rheumatic Fever - inflammatory disease of heart potentially involving all layers Systemic Abnormal immune response to group A beta hemolytic strep (“strep throat”) Transmission to heart via lymphatic channels Most common cause of valvular heart disease
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Rheumatic Fever and Heart Disease
Rheumatic Heart Disease – chronic condition characterized by scarring and deformity of heart valves resulting from rheumatic fever Any or all layers of heart maybe affected
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Rheumatic Fever and Heart Disease
Rheumatic endocarditis (most serious) Erosion and swelling of valves (thickening) Vegetations Stenosis/Regurgitation Rheumatic Myocarditis Nodules and fibrin deposits loss of contractile powerCHF Rheumatic Pericarditis Fibrinous Exudate and pericardial effusion
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Rheumatic Fever and Heart Disease
Nursing Assessment Previous history of rheumatic fever Socioeconomic class Fever Cardiovascular (tachycardia; pericardial friction rub; distant heart sounds; murmurs) Neurological: chorea Skin: subcutaneous nodules and erythema marginatum Musculoskeletal: Polyarthritis
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Rheumatic Fever and Heart Disease
Primary Prevention Detection and treatment of strep throat Secondary Prevention Prophylactic antibiotics to prevent recurrent ARF
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Rheumatic Fever and Heart Disease
Acute Intervention Antibiotics Rest Control Fever Anti-Inflammatories
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Infective Endocarditis
Infection of the inner layer (endocardium) of the heart that usually affects the cardiac valves Was almost always fatal until development of penicillin 5,000-8,000 cases diagnosed in U.S. each year
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Classification Subacute form Longer clinical course Insidious onset
Streptococcus bovis or viridians Staphylococcus epidermidis HACEK group
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Classification Acute form Shorter clinical course Rapid onset
Causative organism more virulent Streptococcus pneumoniae Staphylococcus aureus Streptococcus groups A, B, C Fungi
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Etiology and Pathophysiology
Vegetations Fibrin, leukocytes, and microbes Adhere to the valve or endocardium Embolization of portions of vegetations into circulation
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Bacterial Endocarditis of the Mitral Valve
Fig. 36-2
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Etiology and Pathophysiology
Left-sided more common with bacterial infections and underlying heart disease Right-sided lesions usually caused by IV drug abuse
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Etiology and Pathophysiology
Risk Factors: Cardiac Conditions (blood flow turbulence allows pathogen to infect previously damaged valves or other surfaces) Rheumatic heart disease Prosthetic valves Aging IV drug abuse Invasive Medical and Dental Procedures UTI, skin/wound infections
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Clinical Manifestations
Nonspecific Fever occurs in 90% of patients Chills Weakness Malaise, Fatigue Anorexia
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Clinical Manifestations
Vascular manifestations Splinter hemorrhages in nail beds Petechiae Osler’s nodes on fingers or toes Janeway’s lesions on palms or soles
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Clinical Manifestations
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Clinical Manifestations
Murmur in 80% of cases CHF in up to 80% with aortic valve endocarditis 50% with mitral valve endocarditis Manifestations secondary to embolism
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Sites of Embolization
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HISTORY Recent dental, urologic, surgical, or gynecologic procedures
Heart disease Recent cardiac catheterization Skin, respiratory, or urinary tract infections
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Diagnostic Studies Labs Blood cultures
Echocardiography (detects valvular vegetations, abscesses) Chest x-ray
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Collaborative Care Prophylactic treatment for patients having:
Removal of drainage of infected tissue Indwelling pacemakers Renal dialysis Ventriculoatrial shunts
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Collaborative Care Antibiotic administration Subsequent blood cultures
Monitor antibiotic serum levels Antipyretics Subsequent blood cultures REST Valve repair/replacement
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Nursing Assessment Subjective
History of valvular, congenital, or syphilitic cardiac diseases Previous endocarditis Staph or strep infection Immunosuppressive therapy
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Nursing Assessment Recent surgical procedures or invasive procedures
IV drug abuse Weight changes Chills Diaphoresis
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Nursing Assessment Bloody urine Exercise intolerance
Generalized weakness Fatigue Cough Dyspnea on exertion Night sweats Chest, back, abdominal pain
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Nursing Assessment Objective Olser’s nodes Splinter hemorrhages
Janeway’s lesions Petechiae Clubbing
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Nursing Assessment Tachypnea Crackles Arrhythmias Leukocytosis
Increased ESR and cardiac enzymes Positive cultures ECG showing chamber enlargement
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Nursing Diagnoses Decreased cardiac output Activity intolerance
Ineffective health maintenance
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Acute Pericarditis Caused by inflammation of pericardial sac
Etiologies: Infectious vs Non-Infectious S&S: dyspnea, CP, pericardial friction rub Complications Pericardial effusion Cardiac tamponade Treatment Antibiotics NSAIDS Corticosteroids Positioning head at 45 degree angle Pericardiocentesis
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Valvular Heart Disease
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Valvular Heart Disease
Heart contains two atrioventricular valves and two semilunar valves
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Valvular Heart Disease
Types of valvular heart disease depends on: Valve or valves affected Two types of functional alterations Stenosis Regurgitation
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Valvular Heart Disease
Stenosis Valve orifice is restricted Impending forward blood flow Creates a pressure gradient across open valve Degree of stenosis reflected in pressure gradient differences Regurgitation Incomplete closure of valve leaflets Results in backward flow of blood
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Mitral Valve Stenosis Due to rheumatic heart disease
Causes scarring of valve leaflets and chordae tendineae Contractures develop with adhesions between commissures of the leaflets Stenotic mitral valve assumes funnel shape due to thickening and shortening of valve structures
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Mitral Valve Stenosis Pathophysiology:
Incomplete emptying of LA Increased LA pressure LA dilatation and hypertrophy Increased LA pressureElevated pulmonary pressurepulmonary congestion Incomplete emptying of LAinsufficient volumes to ventricles decreased C.O. Afib is common risk of embolism
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Clinical Manifestations
Dyspnea Occasionally accompanied by hemoptysis Primary symptom because of reduced lung compliance Palpitations from atrial fibrillation Fatigue Opening snap Low-pitched rumbling diastolic murmur Chest pain Seizures (from emboli) Stroke Emboli can arise from stagnant blood in left atrium
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Mitral Valve Regurgitation
Mitral Valve fails to close properly LV ejects blood into aorta and back into LA
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Mitral Valve Regurgitation
Majority of cases attributed to: MI (MI with left ventricular failure places patient at risk for rupture of chordae tendineae) Chronic rheumatic heart disease Isolated rupture of chordae tendineae Mitral valve prolapse Ischemic papillary muscle dysfunction Infectious endocarditis
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Mitral Valve Regurgitation
Acute Onset (e.g. papillary dysfunction due to M.I.) Backward flow increased LA pressure Increased Pulmonary Pressure Pulmonary Edema Chronic Onset Backward flow LA dilates and hypertrophies Increased pulmonary pressures pulmonary congestion right sided failure
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Mitral Valve Regurgitation Clinical Manifestations
Asymptomatic for years until development of some degree of left ventricular failure Initial symptoms include: Weakness Fatigue Dyspnea that gradually progress to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema
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Aortic Valve Stenosis Usually discovered in childhood, adolescence, or young adulthood Those seen later in life usually have aortic stenosis from rheumatic fever or senile fibrocalcific degeneration of a normal valve
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Aortic Valve Stenosis Results in obstruction of flow from LV to aorta during systole Effect is left ventricular hypertrophy and increased myocardial oxygen consumption because of increased myocardial mass Leads to reduced CO and pulmonary hypertension
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Aortic Valve Stenosis Clinical Manifestations
Symptoms of angina pectoris Syncope Heart failure Occurs when valve orifice is 1/3 normal size
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Aortic Valve Stenosis Poor prognosis when experiencing symptoms and valve obstruction is not relieved Why would Nitroglycerine be contraindicated with aortic valve stenosis?
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Aortic Valve Regurgitation
May result from disease of aortic valve leaflets, aortic root, or both Caused by: Bacterial endocarditis Trauma Aortic dissection Constitutes life-threatening emergency Chronic aortic regurgitation results from: Rheumatic heart disease Congenital bicuspid aortic valve Syphilis Chronic rheumatic heart conditions
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Aortic Valve Regurgitation
Physiologic consequence: Retrograde blood flow from ascending aorta to left ventricle Elevated LV pressures LV dilatation and hypertrophy Results in volume overload
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Tricuspid Valve Disease
Tricuspid valve stenosis Seen in IV drug users Right atrial output is obstructed Results in right atrial enlargement and elevated systemic venous pressure
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Tricuspid Valve Disease Clinical Manifestations
Peripheral edema Ascites Hepatomegaly Murmur
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Collaborative Care Drug therapy Digitalis Diuretics Antiarrhythmics
b-blockers Anticoagulants Low-sodium diet
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Collaborative Care Percutaneous transluminal balloon valvuloplasty to split open fused commissures Surgical therapy for valve repair Annuloplasty Valvuloplasty Commissurotomy Valve Replacement Mechanical Vs. Biological
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Nursing Assessment Objective Fever Diaphoresis Peripheral edema
Crackles Wheezes Abnormal heart sounds Ascites Hepatomegaly Cardiomegaly Valve calcification Pulmonary congestion on x-ray
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Nursing Assessment Diagnostic Tests:
Calcification or vegetation of leaflets or prolapse Chamber enlargement Arrhythmias Conduction deficits on ECG
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Nursing Implementation
Prevention of rheumatic valvular disease by diagnosing and treating streptococcal infection and providing prophylactic antibiotics for patients with history Patient with history of endocarditis must also be treated with prophylactic antibiotics
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Nursing Implementation
Teach when to seek medical treatment Design activity to patient’s limitations Discourage smoking Avoid strenuous activity Nursing assessment to monitor effectiveness of medications
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Nursing Implementation
Medic Alert bracelet Teach importance of completing antibiotic regimen Teach drug side effects INR for anticoagualtion therapy Follow-up care
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Case Study Patient Profile: Subjective Data Objective Data
Mrs. S., a 54-year-old Hispanic woman, is admitted to the hospital for valvular heart disease. Subjective Data Was told she had streptococcal throat infection as a child Was diagnosed 10 years ago with rheumatic heart disease Has shortness of breath at rest; cannot get out of bed without becoming dyspneic Takes digoxin (0.25 mg once a day) Objective Data Physical Examination Ankle edema Irregular pulse Crackles at lung bases Murmurs of mitral stenosis, mitral insufficiency, and aortic insufficiency Diagnostic Studies Chest x-ray and ECG indicate enlarged left atrium
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Case Study: Question #1 Explain the cause of Mrs. S.’s valvular heart disease. What valves are most likely to become involved with rheumatic heart disease?
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Case Study: Question #2 Differentiate between the characteristics of mitral stenosis and mitral regurgitation.
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Case Study: Question #3 What other conservative treatment measures might be initiated for Mrs. S. (in addition to digoxin?)
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Case Study: Question #4 On the basis of the assessment data provided, write one or more nursing diagnoses.
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Case Study: Question #5 What are important nursing measures for Mrs. S.?
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