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Comprehensive Study Notes: Infective Endocarditis, Acute Pericarditis, Valvular Heart Disease, and Cardiomyopathy

Infective Endocarditis

  • Definition: infection of the inner layer of the heart that usually affects the cardiac valves; historically almost uniformly fatal until the development of penicillin; approximately 15{,}000 new US cases per year.

  • Anatomy context (brief): The heart wall comprises several layers, including the fibrous pericardium, parietal and visceral serous pericardium, myocardium, and endocardium (as illustrated in Fig. 37-1).

  • Pathophysiology

    • Occurs when blood turbulence within the heart allows a causative organism to infect a previously damaged valve or other endothelial surface.

    • Requires a combination of a susceptible endocardial surface and an infectious agent carried by the blood.

    • Vegetation forms on the valve or endocardium, composed of fibrin, leukocytes, platelets, and microbes; these vegetations can embolize to other sites.

  • Etiology and principal risk factors

    • Common risk factors:

    • Age

    • Intravenous drug use (IVDA)

    • Prosthetic valves

    • Intravascular devices

    • Renal dialysis

  • Vegetation and embolization

    • Vegetations consist of fibrin, leukocytes, platelets, and microbes; they adhere to valve/endocardium.

    • Embolization can disseminate vegetative fragments into systemic circulation (left-sided IE) or pulmonary circulation (right-sided IE).

  • Left-sided vs. right-sided embolization

    • Left-sided IE embolizes to brain, limbs, kidneys, liver, spleen.

    • Right-sided IE embolizes to the lungs, causing pulmonary emboli.

  • Causative organisms

    • Streptococcus viridans (viridans group streptococci)

    • Staphylococcus aureus

    • Viruses

    • Fungi

  • Classification

    • Subacute form: occurs with preexisting valve disease; longer clinical course; insidious onset; commonly caused by enterococci.

    • Acute form: occurs on healthy valves; shorter, rapid onset.

  • Clinical manifestations (nonspecific to specific organism)

    • Fever in about 90\% of patients.

    • Chills, weakness, malaise, fatigue, anorexia.

    • Subacute features: arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headaches, clubbing of fingers.

    • Vascular manifestations: splinter hemorrhages in nail beds; petechiae; Osler’s nodes (fingers or toes); Janeway’s lesions (palms/soles); Roth’s spots (retina).

    • Cardiac findings: murmur in most patients; heart failure can occur in up to 80\% with aortic valve IE; symptoms may be due to embolization.

    • Right-sided IE: embolization to lungs causing pulmonary symptoms/emboli.

  • Diagnosis: history and collaborative testing

    • History highlights: recent dental, urologic, surgical, or gynecologic procedures; prior heart disease; recent catheterization/surgery; intravascular devices; renal dialysis; skin, respiratory, or urinary infections; drug use.

    • Laboratory studies:

    • Blood cultures: two different sites sampled, ~30\text{ minutes} apart; >90\% positivity.

    • WBC count: slightly elevated with differential.

    • Echocardiography: useful; especially when cultures are negative.

    • Chest X-ray: may show cardiomegaly.

  • Collaborative care and treatment

    • Prophylaxis: antibiotic prophylaxis for selected dental procedures, respiratory tract incisions, GI wound infections, urinary tract infections in at-risk patients.

    • Antibiotic therapy: selection guided by culture/sensitivity; common regimens include:

    • Vancomycin and Unasyn (ampicillin/sulbactam), ceftriaxone, Penicillin G if susceptible, nafcillin, depending on organism and prosthetic valve status.

    • Duration: weeks to eradicate the organism; commonly ~6\ \text{weeks} of antibiotics; monitor trough/peak levels and renal function.

    • Prosthetic valve or fungal endocarditis: responds poorly to antibiotics alone; early valve replacement may be adjunct; follow with a prolonged antibiotic course (often 6 weeks).

    • Anticoagulation: increases risk of intracerebral bleed in native valve endocarditis (NVE); if prosthetic valve endocarditis (PVE), anticoagulation may be essential, requiring individualized decisions.

  • Fungal and prosthetic valve IE

    • Requires different management; higher morbidity; often requires surgical intervention.

  • Nursing assessment and planning

    • Subjective data to collect: history of valvular/congenital/syphilitic disease; prior endocarditis; staph/strep infections; immunosuppressive therapy; recent surgeries and procedures.

    • Objective data: vitals, murmurs, signs of emboli, skin findings, digital clubbing, Osler’s nodes, Janeway lesions, Roth’s spots, neurologic changes.

    • Functional assessments and risk factors:

    • IV drug use, alcohol use, weight changes, diaphoresis, exercise intolerance, weakness, fatigue.

    • Diagnostic data: leukocytosis, anemia, elevated ESR/cardiac enzymes, positive blood cultures, echocardiographic evidence of vegetations, ECG changes if present.

  • Nursing implementation and care planning

    • Identify at-risk individuals; assess disease understanding and adherence.

    • Teach infection prevention and antibiotic adherence; stress reducing infection risk; hygiene and following up care.

    • Monitor for nonspecific manifestations and temperature trends to assess treatment success.

    • Monitor IV line patency, renal function, and antibiotic sensitivities.

    • Activity planning: long-term antibiotics (~6\ \text{weeks}) and potential home care; compression stockings if immobile; ROM and respiratory exercises; ambulation as tolerated.

  • Prevention and health promotion

    • Emphasize the importance of preventing streptococcal infections and endocarditis recurrence.

    • Educate on recognition of infection signs and timely medical evaluation.

Acute Pericarditis

  • Definition and context: Inflammation of the pericardial sac; illustrated as acute pericarditis (Fig. 37-4) with shaggy coating of fibrous surface.

  • Etiology and causes (Common causes, table 37-7)

    • Infectious: Viral (Coxsackie A/B, echovirus, adenovirus, mumps, hepatitis, EBV, varicella zoster, HIV); bacterial (pneumococci, staphylococci, streptococci, Neisseria gonorrhoeae, Legionella, gram-negative septicemia); tuberculosis; fungal (Histoplasma, Candida); infections like toxoplasmosis, Lyme disease.

    • Noninfectious: uremia; acute MI; neoplasms (lung/breast cancers, leukemias/lymphomas); trauma (thoracic surgery, pacemaker insertion); radiation; dissecting aortic aneurysm; myxedema; hypersensitive/autoimmune (Dressler syndrome, postpericardiotomy syndrome, rheumatic fever); drug reactions; rheumatologic diseases (RA, SLE, scleroderma, ankylosing spondylitis).

  • Pathophysiology

    • Inflammatory response with neutrophil influx and fibrin deposits on the epicardium.

  • Clinical manifestations

    • Sharp or stabbing chest pain that worsens with inspiration and when supine; pain may radiate to the trapezius.

    • Friction rub detectable on auscultation; best heard with the diaphragm, patient leaning forward, at the lower left sternal border.

  • Diagnostic studies

    • ECG: widespread ST-segment elevation and PR depression (90% of cases show ECG changes); sinus tachycardia common due to pain or pericardial effusion.

    • Laboratory: elevated CRP/ESR and troponins may be present.

    • Imaging: echocardiography; CT/MRI if indicated.

    • Pericardiocentesis may be performed if effusion or tamponade suspected.

  • Complications

    • Pericardial effusion (accumulation of fluid in the pericardial space).

    • Cardiac tamponade (increased pericardial pressure leading to decreased venous return and CO; muffled heart sounds; narrowed pulse pressure).

  • Diagnostic and monitoring tools

    • ECG monitoring during acute episodes; imaging to assess effusion and hemodynamics.

  • Collaborative care and management

    • Treat underlying cause.

    • Anti-inflammatory therapy: NSAIDs; treat infectious etiologies with appropriate antibiotics/antivirals as indicated.

  • Nursing management

    • Pain and anxiety management; bedrest with HOB elevated (about 45^{\circ}); GI protection with proton pump inhibitors; anxiolytics as needed.

    • Monitor for tamponade; prepare for pericardiocentesis if signs develop.

  • Question example (nursing decision-making)

    • If markedly distended JVP, hypotension, muffled heart sounds, tachycardia, tachypnea: tamponade physiology is likely due to excess pericardial fluid restricting diastolic filling.

Valvular Heart Disease

  • Overview

    • Types depend on which valve is affected and the functional alteration (stenosis vs regurgitation).

    • Primary valve disease is often congenital in children/adolescents; adults often have acquired disease (rheumatic disease, degenerative changes, infective endocarditis, etc.).

  • Mitral valve stenosis (MS)

    • Pathophysiology: Narrowed mitral orifice restricts forward flow; creates a pressure gradient across the valve reflecting stenosis severity.

    • Etiology: Historically most often due to rheumatic heart disease; causes scarring and adhesion of leaflets and chordae; potential etiologies include congenital MS, RA, SLE.

    • Morphology: Fish-mouth valve orifice due to thickened, shortened leaflets and commissural fusion.

    • Hemodynamics: Increased left atrial pressure and volume; pulmonary vascular hypertrophy; chronic left atrial pressure elevations.

    • Clinical manifestations: Exertional dyspnea (major complaint due to reduced lung compliance); palpitations due to atrial fibrillation; fatigue; Diastolic murmur.a

    • Additional features: Hoarseness (laryngeal nerve impingement), hemoptysis (pulmonary hypertension), chest pain, seizures, embolic strokes.

  • Mitral valve regurgitation (MR)

    • Valve function depends on intact leaflets, annulus, chordae tendineae, papillary muscles; patency depends on left atrium and left ventricle and their function.

    • Common etiologies: MI, chronic rheumatic disease, mitral valve prolapse, ischemic papillary muscle dysfunction, infective endocarditis.

    • Clinical manifestations:

    • Acute MR: thready peripheral pulses, cool/clammy extremities due to sudden CO drop.

    • Chronic MR: often asymptomatic for years; signs of left-sided failure eventually; left-sided murmur may be masked by low CO; rapid assessment essential.

    • Initial symptoms: weakness, fatigue, palpitations, dyspnea progressing to orthopnea, PND, peripheral edema.

    • Auscultation: loud, long, pansystolic/holosystolic murmur at the apex radiating to the left axilla; S3 due to increased LV filling.

  • Mitral valve prolapse (MVP)

    • Definition: abnormality of mitral leaflets and papillary muscles/chordae tendineae; leaflets prolapse into the left atrium during systole; etiology often unknown with possible genetic predisposition; may occur with other hereditary conditions.

    • Diagnostic appearance: MVP on imaging with hooding of leaflets.

    • Clinical course: usually benign but can have complications including MR, IE, sudden death, heart failure, cerebral ischemia.

    • Clinical manifestations: Many patients asymptomatic; ~10% develop symptoms including murmur that intensifies during systole, late systolic murmur, and mid-to-late systolic clicks; dysrhythmias (PVCs, PSVT), palpitations, lightheadedness, dizziness.

  • Aortic valve stenosis (AS)

    • Epidemiology: Often diagnosed in childhood/adolescence/young adulthood; late-onset AS typically due to rheumatic disease or degenerative calcific changes.

    • Pathophysiology: Obstruction of flow from left ventricle to aorta during systole; leads to LV hypertrophy and increased myocardial oxygen demand.

    • Consequences: Reduced CO, pulmonary hypertension.

    • Clinical manifestations: Angina, syncope, exertional dyspnea (classic triad).

    • Prognosis and pharmacology: Poor prognosis once symptoms and obstruction develop; nitroglycerin is contraindicated due to preload reduction.

  • Aortic valve regurgitation (AR)

    • Etiology: Disease of aortic valve leaflets or aortic root; causes include infective endocarditis, trauma, aortic dissection; other etiologies include rheumatic disease, bicuspid valve, syphilis.

    • Hemodynamics: Retrograde flow from the aorta into the left ventricle causing volume overload; early compensated dilation and hypertrophy of the LV; progressive decline in contractility.

    • Acute vs chronic: Acute AR presents with sudden cardiovascular collapse; chronic AR may be asymptomatic for years with exertional dyspnea, orthopnea, PND.

    • Signs: Soft or absent S1; S3 and S4; soft, high-pitched diastolic murmur; Austin Flint murmur.

  • Diagnostic studies for valvular disease

    • History and physical exam; chest radiography; ECG; echocardiography; cardiac catheterization may be used to assess hemodynamics and CAD.

  • Management and preventive care

    • Percutaneous/transcatheter approaches: Balloon valvuloplasty to split fused commissures (mitral stenosis) or other valvuloplasty techniques as indicated.

    • Surgical: Valve repair preferred when feasible; valve replacement for selected patients.

    • Prosthetic valve types (examples): Starr-Edwards caged-ball valve; St. Jude bi-leaflet valve; Carpentier-Edwards porcine valve.

    • Prophylaxis and lifestyle: Prevention of recurrent rheumatic fever and endocarditis; discourage smoking; activity design based on limitations; medical alert bracelets.

  • Nursing assessment and planning (valvular disease)

    • Objective data: hepatomegaly, diaphoresis, peripheral edema, ascites; crackles, wheezes, hoarseness; abnormal heart sounds; tachycardia; dysrhythmias; hypotension.

    • Activity and ADLs goals: energy conservation; avoid excessive fatigue; implement rest periods.

    • Education: medication adherence, wound care if surgery, bleeding precautions with anticoagulants, recognizing signs of decompensation.

    • Pharmacological RX: Digitalis (Positive Inotropes)

  • Prevention and patient education

    • Emphasize antibiotic prophylaxis for dental procedures and other risk periods; lifestyle changes to reduce infection risk; regular follow-up for valve function.

Cardiomyopathy (CMP)

  • Definition and overview

    • Group of diseases affecting structure and function of the myocardium; defined by clinical manifestations and diagnostic procedures; three major categories: dilated, hypertrophic, restrictive.

  • Dilated cardiomyopathy (DCM)

    • Etiology/pathophysiology: Most common CMP; HF in 25\% - 40\% of cases; often follows infectious myocarditis; inflammation and degeneration with ventricular dilation; impaired systolic function; atrial enlargement and stasis of blood.

    • Prognosis: Sudden cardiac death (SCD) from ventricular dysrhythmias is a leading cause of death; cardiomegaly due to dilation; contractile dysfunction despite large chamber size.

    • Clinical manifestations: HF symptoms; decreased exercise capacity; fatigue; dyspnea at rest; orthopnea; dry cough; palpitations; bloating; irregular heartbeat; S3/S4.

    • Diagnostics: History; Doppler echocardiography to distinguish CMP from other abnormalities; CXR showing cardiomegaly and pulmonary venous HTN; ECG with tachy/brady and conduction disturbances; BNP elevated with HF; cardiac cath to assess CAD.

    • Management: Control HF by improving contractility (preload reduction with nitrates; diuretics to reduce preload; afterload reduction with ACE inhibitors); neurohormonal blockade (beta-blockers like Lopressor; aldosterone antagonists such as spironolactone); consider anticoagulants to reduce embolic risk in the setting of A-fib; mechanical support (VAD) as needed; transplant consideration with advanced disease.

  • Hypertrophic cardiomyopathy (HCM)

    • Definition: Asymmetric LV hypertrophy without LV dilation; often genetic; common in young adults and athletes; most common cause of SCD in healthy young people.

    • Pathophysiology and anatomy: Massive LV hypertrophy with small LV cavity; rapid, forceful contraction; impaired relaxation (diastolic dysfunction); possible outflow tract obstruction.

    • Clinical manifestations: May be asymptomatic; exertional dyspnea; fatigue; angina; dysrhythmias (SVT, AF, VT, VF); risk of sudden death especially with strenuous activity.

    • Management goals: Improve ventricular filling; relieve outflow obstruction; pharmacologic therapy (beta-blockers, calcium channel blockers); digitalis for inotropy and antiarrhythmic support; antiarrhythmics (amiodarone or sotalol) in arrhythmias; pacing in select cases.

  • Restrictive cardiomyopathy (RCM)

    • Etiology/pathophysiology: Least common CMP; impaired diastolic filling with relatively preserved systolic function; myocardial fibrosis and stiff noncompliant ventricle; may be due to amyloidosis, sarcoidosis, hemochromatosis, post-radiation fibrosis, endocardial fibroelastosis, etc.

    • Clinical manifestations: Fatigue, exercise intolerance, dyspnea due to limited CO increase; angina; orthopnea; syncope; palpitations.

    • Diagnostics: Chest X-ray may be normal or show cardiomegaly with pleural effusion; signs of pulmonary congestion; ECG may show tachyarrhythmias including AV block; progression to HF.

  • Additional notes and educational points

    • Some slides include mnemonic or creative aids (e.g., “Creative-Med-Doses” for CMP etiologies) to aid memory.

    • VAD as a bridge to transplantation or destination therapy in advanced dilated CMP.

  • Nursing considerations and planning (CMP)

    • Monitor for HF symptoms and arrhythmias; assess signs of poor perfusion and fluid status; monitor for thromboembolism in AF; education on activity modification and medication adherence; consider genetic counseling for HCM.

  • Bottom line for CMP management

    • Goals focus on symptom relief, delaying progression, managing HF, preventing sudden death in high-risk patients, and considering advanced therapies (ICD, transplant) when appropriate.

Quick reference: Key numbers, signs, and concepts

  • IE incidence: 15{,}000 new cases/year in the United States.

  • Fever prevalence in IE: 90\%.

  • Systemic embolization in IE: up to 50\% of patients.

  • IE treatment duration: typically 6\ \text{weeks} of antibiotics.

  • Acute pericarditis ECG finding: diffuse ST elevation with PR depression.

  • Atrioventricular conduction changes and rhythm disturbances are common in CMP discussions (AF, VT, VVT).

  • Major CMP categories: Dilated, Hypertrophic, Restrictive.

Connections to foundational concepts and real-world relevance

  • Endocarditis demonstrates how hemodynamics (valve damage, turbulent flow) enables infection to establish on valvular structures, highlighting the interplay between anatomy, infection, and embolic risk.

  • Pericarditis emphasizes inflammatory processes around the heart and the spectrum from inflammation to tamponade, with diagnostic importance of ECG and imaging.

  • Valvular heart disease shows how structural changes (stenosis vs regurgitation) alter pressures and volumes, with sequelae like LV hypertrophy, pulmonary hypertension, and HF; management often involves interventional cardiology (balloon valvuloplasty) or surgery.

  • Cardiomyopathy illustrates primary myocardial diseases independent of valvular defects, where treatment targets myocardial function, arrhythmia risk, and, in advanced disease, transplantation or mechanical support.

Formulas and numerical references ( LaTeX formatted)

  • Incidence and prevalence figures:

    • 15{,}000 new cases/year (Infective Endocarditis).

    • 90\% of IE patients exhibit fever.

    • 50\% of IE patients experience systemic embolization.

  • Treatment duration:

    • 6\ \text{weeks} of antibiotics for endocarditis.

  • Hemodynamic concepts (described in text):

    • Mitral stenosis involves a pressure gradient across the valve; the degree of gradient reflects stenosis severity: Delta P = P{LA} - P{LV} across the mitral valve during diastole (conceptual; not explicitly stated in the transcript).

  • Clinical thresholds described (examples):

    • Angina, syncope, and exertional dyspnea triad in aortic stenosis; represented as a progression of LV failure symptoms (no explicit numeric thresholds given in the transcript).

Suggested study prompts (to test comprehension)

  • Compare and contrast subacute vs acute infective endocarditis in terms of valve condition, clinical course, and typical organisms.

  • List the vascular and immunologic signs of IE and describe how they might guide diagnosis.

  • Describe the pathophysiology of cardiac tamponade and explain how it would present clinically.

  • Outline the standard management approach for rheumatic Mitral Stenosis and how Balloon Valvuloplasty can alter hemodynamics.

  • Explain the distinguishing features and clinical significance of Hypertrophic Cardiomyopathy compared with Dilated CMP.

  • Identify key diagnostic tests for valvular heart disease and what each test contributes to management decisions.