Traumatic, Inflammatory, Infectious Heart Disease PDF

Summary

This document discusses different types of heart diseases, including inflammatory, infectious, and traumatic conditions. It covers causes, signs, symptoms, diagnosis, and treatment options. The information is relevant to medical professionals.

Full Transcript

Endocarditis What ​ Inflammation of inner lining of the heart and the valves ○​ Infective: inflammation or infection affecting heart valves ​ MOST COMMON (M>W)...

Endocarditis What ​ Inflammation of inner lining of the heart and the valves ○​ Infective: inflammation or infection affecting heart valves ​ MOST COMMON (M>W) ○​ non infective: formation of sterile platelet and fibrin thrombi ​ RARE- found on autopsy Cause ​ Infective: staph, strep viridans (s/p dental), strep pneumo, HACEK, fungi (candida/asp) ○​ Damage to endothelium causes platelets/fibrin deposits which adhere bacteria that invade to cause inflammation and destroy valves ​ Non infective: Rheumatic endocarditis- impacts MV > AV ○​ Endothelial injury to leaflets, platelet activation/deposition, thrombus Classifying endocarditis: ​ Acute infectious (sudden *staph) vs Subacute infections (gradual onset *s viridans) ​ Native valve (community, IV drug use, staph/strep) vs Prosthetic valve ​ Left sided vs right sided (IV tri drugs) Note: vegetations are masses that form due to infection/inflammation s/p damage and can cause emboli- both d/t fibin/plt Signs/Sx Sx: more common to IE than NIE ​ Fever ?, night sweats, fatigue, loss of appetite, weight loss, myalgias/arthralgias FROM JANE PE: ​ New or changing murmur (MR, TR, AR), tachy, arrhythmia (d/t spread of infection disrupt conduction) ​ Splinter hemorrhages (microthrombi) ​ Osler nodes (red nodes on fingers/toes) ​ Janeway lesions (small, painless, erythematous lesions on palms and soles) ​ Roth spots Diagnosis ​ Echo: TTE vs TEE ○​ TTE initial ○​ TEE if TTE is negative and still suspicious ​ Labs: ○​ inflammatory markers: ESR and CRP elevated ○​ CBC: leukocytosis, normocytic anemia ​ Blood culture: 3 samples from different sites obtained prior to starting abx (- dont r/o endo) ​ ECG: usually normal- baseline tracing and could ID heart block or bundle branch block ​ CXR: R/O other causes of sx- but in endocarditis: septic emboli or pulm edema, cardiomegaly ​ CT: metastatic infection ​ MRI: if concerned for cerebral embolic events NIE: antinuclear antibodies, lupus anticoags, antiphospholipid antibodies Duke criteria: 2 major, 1 major + 3 minor, 5 minor Treatment Infective ​ Patients get admitted and start empiric abx and Consult ID, cardiology, CT surgery ○​ Native valve: Vanco + gent or ceftriaxone | Niaficilin + gent ○​ Prosthetic valve: Vanco + gent + rifampin ​ Meds for 4-6 weeks ​ Blood cultures repeated q24 hrs ​ Continuous PE ​ Discharge once hemodynamically stable, negative blood culture, sx was consulted ○​ Discuss outpt IV therapy Noninfective ​ tx underlying condition + anticoags Surgical management ​ Valve repair for: HF, persistent infection, embolic events, conduction abnormalities ​ Pacemaker needed if: sepsis, pocket infection, persistent infection, staph bacterimia Need abx b4 dental work Prophylaxis for valves, congenital defects/disease of heart (amox, ceph, clinda) risks Noninfective: ​ trauma, circulating immune complexes, cytokines, antigen-antibody relations ​ Hypercoagulable state ​ Thrombus Infective: heart disease (rheumatic, congenital), 60>, IV drug user, immunocomp, prior hx, poor dentition Complications Cardiac: perivalvular, valve insufficiency, valve rupture, HF, pericarditis Renal: glomerulonephritis, antibiotic induced nephrotoxicity Metastatic infections and death Pericarditis What ​ Inflammation of the pericardium, double layer sac surrounding the heart ​ Classification: based on duration ○​ Acute 6mo (constrictive, adhesive) ​ Common to young men Cause ​ Idiopathic: ○​ CP 1-2 weeks after infection ​ Viral infection: coxsackievirus B (see above) ​ Bacterial infection: TB, rheumatic fever ○​ + culture or bx reveals caseating granuloma ​ Cardiovascular: Dressler syndrome (post MI) ○​ 1-4 weeks after operation/injury ​ Cancers or meds ​ Fungal is rare Signs/Sx Acute Pain: severe, sharp, pleuritic, steady pain that can radiate to neck, shoulder, arm, trapezius ​ Worsens when lying supine + coughing ​ Improves when leaning forward PE: ​ Neck vein distention, pericardial friction rub (heard w/expiration and leaning forward) Chronic pain: less severe, could be absent if slowly developing ​ May have dyspnea (SOB) PE: ​ May have neck vein distention ​ X ray: large cardiac silhouette Diagnosis ​ EKG: ○​ Acute: Diffuse ST segment elevation w/ upward concavity and w/o T wave inversions ○​ PR depressions ○​ Chronic: electrical alternans (QRS amplitude alternate) with a large effusion ○​ EKG findings happen in both due to inflammation of atria disrupt conduction ​ Echo: ○​ Isolated: normal ○​ Acute and chronic: Pleural effusion (fluid in between layers of pericardium) ​ Blood: may show nonspecific- inc ESR, CRP, leukocytosis Treatment Viral or idiopathic ​ O2 and analgesia (can be tx on outpt basis with NSAIDS or high dose ASA x 7-14 days) ​ KNOW: NSAID and colchicine 7-14 days + gastric protection ○​ Colchicine enhances response and decreases recurrence rate ​ If no improvement w/ above- use STEROIDS When to admit: fever, tamponade/effusion, immunosuppressed, ↑ troponin: intense dialysis, abx, tb tx Complications Cardiac tamponade, pericardial effusion, constrictive pericarditis Constrictive pericarditis: thickened/scarred pericardial sac that lies around heart and prevents proper diastolic filling ​ Cant fill properly so more venous pressure leading to decreased SV ​ Slow onset: dyspnea, fatigue, orthopnea, cough, weight gain, right sided HF, JVD/edema, pericardial knock (high pitched 3rd sound) ​ CXR: pericardial calcification ​ ECHO: pericardial thickening ​ EKG: low voltage QRS, afib ​ TX: surgery- resection of pericardial is only definitive tx and use diuretics before sx 6 Ps: pleuritic, persistent, positional, cP, pericardial friction rub, PR depressions Pericardial effusion and cardiac tamponade What ​ PE: Accumulation of fluid in pericardial space ○​ 2/2 pericarditis, uremia, cardiac trauma ​ CT: rapid accumulation of pericardial fluid/pericardial effusion to impaired cardiac filling and cause hemodynamic compromise ○​ Occurs in pericardial sac ○​ Common to boys/men Cause ​ Viral- most common (coxsackie, influenza,HIV, EBV, CMV) ​ Bacteria (staph, strep, neisseria, legionella) ​ Fungal ​ Malignancy ​ Trauma, post procedure ​ Autoimmune (SLE, RA) ​ Meds (hydralazine, minoxidil, anticoags) Whats happening: normal fluid exists- but when there is too much, it ↑ pressure and compresses heart ​ ↓ diastolic filling, SV, CO ​ ↑ HR to maintain CO Rapid filling of fluid= tamponade Signs/Sx With tamponade ​ Dyspnea, cough, CP, lightheaded, syncope, palpitations, hoarseness, fatigue Triad CT: JVD, W/O tamponade muffled sounds, ​ Usually no sx- but if sx usually related to underlying cause (infection, autoimmune etc) hypoTN, pulse weak PE: ​ Vitals: hypotn, tachy ​ Cards: pericardial friction rub, muffled heart sounds, JVD, hepatojugular reflux, weak peripheral pulse, pulsus p ​ Resp: dullness to percussion/diminished breath sounds Diagnosis ​ EKG: sinus tachy, low voltage QRS, diffuse ST elevation w/PR depression, electrical alternans (qrs alt height) ​ CXR: enlarged cardiac silhouette when >250mL fluid ​ TEE: diagnostic test of choice ○​ Pericardial effusion: echolucent space in pericardial sac ○​ CT: R atrial free wall collapse during Systole and RV wall collapse during Diastole. IVC dilated ​ Pericardial fluid analysis/bx but not common ​ Labs: CBC, BUN/Cr, ESR, CRP, ANA, TSH, quantiFERON, HIV Treatment PE ​ Depends on stability and underlying cause- tx pericarditis like above ​ Small effusions are self resolving ​ Drain for large (pericardiocentesis) CT ​ Admin O2, IV fluids, pericardiocentesis Surgery: bx, pericardiotomy or window Myocarditis What ​ Inflammatory disease of the myocardium ○​ Affects young men and young adults more Cause ​ Idiopathic ​ Infections: virus (coxsackie B), bacterial, protozoal, fungal ​ Immune mediated disorder: rheum fever, SLE, allergic reactions, sarcoid/scleroderma ​ Genetics ​ Env: black widow venom ​ Drugs: cocaine, amphetamines, ethanol Whats happening: inflammation causes heart to enlarge and dilate the chambers- this injures myocytes ​ Viral toxicity or bacterial invasion or autoantibodies etc ​ Essentially lead to inflammation/injury, tissue dies ​ Severe can lead to fibrosis and chamber remodeling- DCM Issues lead to HF, arrhythmias, pericarditis Signs/Sx ​ Classify based on sx onset/progression: subclinical, acute, chronic ​ Sx: fever, CP, orthopnea, loss of appetite, fatigue, abdominal pain, decreased exercise PE: heart failure signs ​ Tachy, arrhythmias, peripheral edema, hepatomegaly, JVD, murmurs (MR/TR), S3/S4 gallops, pericardial rub Diagnosis ​ EKG: nonspecific ST changes, arrhythmias, conduction delays ​ CXR: cardiomegaly ○​ HF indications (pulm venous congestion, pleural effusion) ​ Echo: Can be normal in early or mild disease ○​ LV dilation, Ventricular systolic dysfunction, MR/TR, pericardial effusion, intracardiac thrombi ​ Labs: ESR, CRP, troponin + CK MB, natriuretic peptide, rheumatologic screening ​ Cardiac MRI: shows enhancement of myocardial wall ​ Endomyocardial bx: gold standard (rare tho) ○​ Cellular infiltrates: lymphocytic, eosinophilic, neutrophilic, mononuclear Treatment ​ Supportive mainstay- tx HF, arrhythmias, fix any underlying cause ​ Meds: diuretics, ACEI, BB, Angiotensin 2 blockers ​ Intense HF: balloon pump, LVAD, transplant ​ Tx arrhythmias; cardioversion, meds, pacing ​ Anticoags?? AVOID: NSAIDS, alcohol, exercise

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