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NCM 112 SEMI FI LEC by TONS and MADS CARDIOVASCULAR CM TOPICS I. INFECTIOUS DISEASES OF THE HEART ➔ Any of heart’s 3 layers affected by infectious process. ➔ Rheumatic endocarditis - unique infective endocarditis syndrome. ➔ Diagnosis of infection: symptoms and echocardiography. ➔ Ideal management: prevention, IV antibiotics Rheumatic Endocarditis vs Infective Endocarditis Rheumatic Endocarditis Infective Endocarditis Etiology Rheumatic fever Bacterial or fungal infections Pathogenesis Autoimmune response to group A Streptococcus Infection of the heart valves by microorganisms Microbial Involvement Not primarily infectious Primary infection-driven condition Valve Involvement Mitral valve most commonly affected Affects various heart valves, including mitral, aortic, tricuspid, and pulmonary Preexisting Heart Condition Often associated with prior episodes of rheumatic fever Can occur in individuals with or without preexisting heart conditions Fever Low-grade or absent High fever is common Systemic Symptoms Generally mild systemic symptoms Severe systemic symptoms, including sepsis, embolic phenomena, and organ involvement Laboratory Findings Elevated ESR (Erythrocyte Sedimentation Rate) and CRP (C-Reactive Protein) Positive blood cultures, elevated ESR, CRP, and other inflammatory markers Diagnosis Based on clinical presentation, history of rheumatic fever, and echocardiography Blood cultures, echocardiography, and other imaging techniques Treatment Anti-inflammatory drugs: NSAIDs and corticosteroids to control inflammation Antibiotics to treat the underlying infection, and in severe cases, surgical valve repair or replacement Complications Chronic valvular damage and potential for recurrence Embolic events, sepsis, and severe cardiac damage if not promptly treated Prevention Preventing rheumatic fever through streptococcal infection prophylaxis Good hygiene, dental care, and addressing risk factors like IV drug use Prognosis Generally better long-term prognosis Can be life-threatening if not treated promptly Comparison of Myocarditis, Pericarditis, and Endocarditis Name Myocarditis Pericarditis Endocarditis Location Inflammation of myocardium (heart muscle) Inflammation of pericardium (membrane surrounding the heart) Inflammation of the endocardium (inner lining of the heart chambers) Primary Cause Often viral infections (entero/adenoviruses) but can also be caused by bacteria, fungi, or autoimmune diseases Often viral infections ( Coxsackie virus) but can also result from bacterial or autoimmune causes Primarily caused by bacterial or fungal infections, rarely by autoimmune disorders Symptom Chest pain, SOB, fatigue, palpitations, and heart rhythm disturbances Sharp chest pain that worsens with breathing or lying down, fever, and general malaise Fever, heart murmurs, fatigue, night sweats, and signs of systemic infection Diagnosis Echocardiography, cardiac MRI, endomyocardial biopsy Echocardiography, ECG, chest X-ray, and pericardial fluid analysis Blood cultures, echocardiography, transesophageal echocardiography, and Duke criteria Treatment Supportive care, rest, heart medications, and treatment of underlying cause NSAIDs, colchicine, and, in severe cases, pericardiocentesis Antibiotics to treat the infection, and in some cases, surgical valve repair or replacement Complicat ions Heart failure, arrhythmias, and cardiomyopathy Cardiac tamponade (fluid accumulation) Embolic events,HF, valve damage, and systemic complications Prognosis Can range from mild and self-limiting to severe and chronic Generally good with proper treatment, but complications can occur Prognosis varies depending on the cause, promptness of treatment, and extent of heart damage A. Rheumatic Endocarditis 1. Acute rheumatic fever (most often in schoolage) may develop after episode of group A betahemolytic streptococcal pharyngitis a) Rheumatic fever (preventable disease) S/S: Fever, ChillsSore throat (sudden), Diffuse redness of throat with exudate on oropharynx (may not appear until after first day), Enlarged and tender lymph nodes, Abdominal pain (common in children), Acute sinusitis and acute otitis media (cause or from streptococcal pharyngitis) b) Penicillin - most common antibiotic prescribed. 2. Rheumatic fever → rheumatic heart (new heart murmur, cardiomegaly, pericarditis, and HF) 3. Prompt treatment of “strep” throat with antibiotics can prevent development of rheumatic fever. 4. Streptococcus is spread by direct contact with oral or respiratory secretions. Although bacteria are the causative agents, malnutrition, overcrowding, poor hygiene, and lower socioeconomic status may predispose individuals to rheumatic fever. B. Infective Endocarditis 1. Microbial infection of endothelial surface of heart. 2. Usually develops in people with prosthetic heart valves or structural cardiac defects (valve disorders, HCM) 3. Risk Factors: a) Prosthetic cardiac valves or prosthetic material used for cardiac valve repair b) History of bacterial endocarditis (even without heart disease) c) Congenital heart disease d) Unrepaired cyanotic congenital heart disease, palliative shunts and conduits e) aw Repaired congenital heart disease w/ prosthetic material/device by surgery/catheter intervention during first 6 mos after procedure f) Repaired congenital heart disease with residual defects at site or adjacent to site of prosthetic patch or device g) Cardiac transplant recipients with valvulopathy 4. More common in older people, who are more likely to have degenerative or calcific valve lesions, ↓ immunologic response, metabolic alterations 5. Staphylococcal endocarditis of righ valves common among IV injection drug users. 6. Hospital-acquired most often in patients with debilitating disease or indwelling catheters, hemodialysis or prolonged IVF or antibiotic therapy. 7. Fungal endocarditis: immunosuppressive medications or corticosteroids 8. Invasive procedures (esp involving mucosal surfaces) can cause a bacteremia → (if any anatomic cardiac defects) → bacterial endocarditis. 9. ↑incidence from ↑IV injection drug abuse and body piercing, especially oral, nasal, and nipple piercings 10. Pathophysiology a) Deformity or injury of endocardium → accumulation on endocardium of fibrin & platelets (clot formation) → organism (staphylo/strepto/entero/pneumococci or chlamydia, invade clot and endocardial lesion b) Other: fungi (Candida, Aspergillus) & Rickettsiae. 1

NCM 112 SEMI FI LEC by TONS and MADS b) Parenteral administered in doses that produce high serum concentration for significant period to ensure eradication of dormant bacteria within dense vegetations. c) Serum levels of antibiotic monitored. If ↓bactericidal → ↑dosages or different antibiotic d) Penicillin - medication of choice. e) Blood cultures monitor effect of therapy. f) Fungal endocarditis: antifungal amphotericin B (Abelcet, Amphocin, Fungizone) g) Temp monitored; course of fever is one indication of effectiveness of treatment. However, febrile reactions may occur as result of medication. 15. Surgical Management a) if infection does not respond to medications, patient has prosthetic heart valve endocarditis, has vegetation >1cm, or develops complications (septal perforation) b) Valve débridement or excision, débridement of vegetations, débridement/closure of abscess, and closure of a fistula. c) Aortic/mitral valve débridement, excision, or replacement in patients who: (1) Develop congestive HF despite treatment (2) Have >1 serious systemic embolic episode (3) Develop valve obstruction (4) Develop periannular (heart valve), myocardial, or aortic abscess (5) Have uncontrolled infection, persistent or recurrent infection, or fungal endocarditis d) Surgical valve replacement greatly improves prognosis. The aortic valve best treated with autograft. Most patients who have prosthetic valve endocarditis (infected valve replacements) require valve replacement. 16. Nursing Management a) Monitor temperature, Heart sounds (new or worsening murmur indicate dehiscence ofprosthetic valve, rupture of abscess, or injury to valve leaflets or chordae tendineae) b) Monitor S/S of systemic embolization, pulmonary infarction and infiltrates, organ damage (stroke, CVA, brain attack), meningitis, HF, MI, glomerulonephritis, splenomegaly. c) All invasive lines and wounds assessed for redness, tenderness, warmth, swelling, drainage, or other signs of infection. C. Myocarditis 1. Inflammatory process involving myocardium 2. Can cause heart dilation, thrombi on heart wall (mural thrombi), infiltration of circulating blood cells around coronary vessels and between muscle fibers, and degeneration of muscle fibers 3. Mortality varies with severity of symptoms. a) Mild symptoms recover completely; else cardiomyopathy and HF. 4. Pathophysiology a) Usually results from viral (coxsackievirus A/B, HIV, influenza A), bacterial, rickettsial, fungal, parasitic, metazoal, protozoal (Chagas disease), or spirochetal infection. b) It also may be immune related, occurring after acute systemic infections (rheumatic fever_ c) May develop in: immunosuppressive, endocarditis, Crohn disease, or SLE, inflammatory reaction to toxins (pharmacologic agents like anthracyclines for cancer therapy), ethanol, or radiation (especially to left chest or upper back). d) May begin in one small area of myocardium and then spread throughout the myocardium. e) Degree of myocardial inflammation and necrosis determines degree of interstitial collagen and elastin destruction. (1) Greater destruction → greater hemodynamic effect f) DCM & HCM are latent manifestations 5. Clinical Manifestations - Depend on type of infection, degree of damage, & capacity of myocardium to recover. a) May be asymptomatic, with infection that resolves on its own. b) May develop mild to moderate symptoms: fatigue, dyspnea, palpitations, and occasional discomfort in chest and upper abdomen. c) Most common: flulike. d) Sudden cardiac death or quickly develop severe CHF 6. Assessment and Diagnostic Findings a) Assessment may reveal no abnormalities; can go undiagnosed. b) Tachycardic, chest pain (with a subsequent cardiac catheterization demonstrating normal coronary arteries). c) Cardiac MRI with contrast - diagnostic guide to sites for endocardial biopsies for organism/ genome, immune process or radiation reaction d) W/o abnormal heart structure may suddenly develop dysrhythmias or ST–T-wave changes. e) If patient has structural heart abnormalities” cardiac enlargement, faint heart sounds (esp S1), a gallop rhythm, or a systolic murmur. f) ↑WBC and ↑ESR 7. Prevention: Prevention of infectious diseases by appropriate immunizations (eg, influenza, hepatitis) and early treatment appears 8. Medical Management a) Specific treatment for underlying cause: penicillin for hemolytic streptococci b) Bed rest to decrease cardiac workloa .& decrease myocardial damage & complications c) In young patients with myocarditis, activities should be limited for 6-month period or at until heart size and function returned to normal. d) Physical activity is increased slowly and instructed to report any symptoms that occur with increasing activity e) If HF or dysrhythmia develops: all management but beta-blockers avoided because they decrease strength of ventricular contraction (negative inotropic effect). 9. Nursing Management a) CV assessment focus: HF and dysrhythmias. b) Dysrhythmias: continuous cardiac monitoring c) 3

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