Endocarditis notes - infective PDF

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Summary

Infective endocarditis - patho, treatment, s/s...

Description

Endocarditis Inflammation of endocardium. Valves usually

affected.

Onset: Organism

Acute Infective Sudden Staph aureus

Risk factors

IV drug use, infected IV site

Patho process

Rapid valve destruction

Presentation

Spiking fever, chills, HF manifestations

Manifestations:

Subacute infective Gradual Strep viridans, fungi, yeast, enterococci Damaged heart, dental work, invasive procedure, infection Valve destruction leading to regurg, embolization of friable vegs Febrile illness with cough, dyspnea, arthralgia, abd pain Fever,

fragments

HF

Abscesses Aneurysms Diagnosis: Blood cultures: + when cultures 12h apart from 2 sites taken are + Echo: visualize vegetations Serologic immune testing: circulating antigens to assess for typical infective agents Treatment:

chills, HA General malaise, fatigue

Provide supportive care, give extended course of

Arthralgias Weight loss, anorexia, abd pain SHOB, dyspnea, cough alert for:

Complications: Embolization of vegetative

Be

Petechiae Janeway lesions (macular lesions on palms/ soles of feet) Osler’s nodes (reddened painful growths on finger/toe pads) Roth’s spots (whitish spots seen on retina) Ominous sign: NEW OR CHANGING CARDIAC MURMUR, S/S OF HF

ABX and prevent complications Valve replacement surgery: HS more common with infections in the aortic valve than mitral/tricuspid valves Pt should take ABX before procedures (dental, surgery) and wear med-alert bracelet

Entry of a pathogen into the bloodstream;

platelet fibrin vegetation formed on damaged endothelium. Organisms colonize vegetations and they enlarge as platelets and fibrin go to site to cover infecting organism. This covering allows pathogen to hide from immune system. Friable vegetations may shear off and embolize. Ultimately vegetations scar and deform valve and cause turbulence in heart as valve function is affected. Myocarditis Inflammation of the heart muscle resulting from an infectious process or immunologic response d/t effects of radiation, toxins, drugs. Myocardial cells are damaged by an inflammatory response that causes local or diffuse swelling and damage. Abscesses formed by infectious agents.

Manifestations: Recent URI, fever, chills, SHOB, chest pain, fatigue, sore throat Be alert for: JVD, bilateral crackles, peripheral edema, low CO, left ventricular failure Ominous sign: untreated, MI, ischemia, dilated Risk if factors: cardiomyopathy, dysrhythmias, HF, sudden Male Malnutrition death ETOH use Immunosuppressives

Immune system destroys Treatment: myocardial cells while destroying pathogen. Usually self-limited; Focus on resolving inflammatory process! may Antimicrobialbecome therapychronic and lead to dilated cardiomyopathy. Antiviral therapy with interferon Severe state may lead to HF Corticosteroids ACEs for HF Digoxin used with caution Diagnosis: Antidysrhythmics CXR: Enlarged heart, fluid in lungs Anticoagulants 12 lead ST segment BedrestEKG: and arrhythmias, reduced activity 6m-1y ad T

Pericarditis and Complications

Collagen vascular disease Aortic aneurysm

Dressler’s syndrome (after surgery)

Pathophys:

Signs/Symptoms:

Pericardial tissue damage is caused by inflammatory response Diagnosis:

Constant,Treatment: sharp chest pain made worse by breathing. Alleviated when up and leaning forward. Monitor patient, keep on bed rest, give O2 Pericardial friction rub (50%) NSAIDs or prednisone; if caused by infection, give Fever – low grade ABX or antifungal Dyspnea and tachycardia Provide dialysis for ESRD May need pericardiectomy (if disease recurs over 2

with capillary permeability ↑ and ECG: diffuse ST elevation in all leads fluid exudate formed in the sac. Echo—look for tamponade or effusion This may cause scarring and CXR: Rule out pulmonary pathology restrict cardiac function. CT scan: identify Chronic pericarditis will cause pericardial effusion vs constrictive i di i idit pericarditis Pericardiocentesis: determine source of effusion Labs: Troponin, CBC, blood culture, Creactive protein, sedimentation rate; may do BUN/Creatinine to check renal fxn, HIV/TB testing, cardiac enzymes

years) or pericardial window to allow fluid to drain Tel pt to restrict activities and avoid vigorous exercise

Pericardial effusion: abnormal collection of fluid between the pericardial layers that threatens normal cardiac function. Could be blood, pus, serum, lymph, or a combination. Normal fluid: 30-50ml. Can stretch slowly to hold 2L without adverse effects or intervention. Rapid accumulation 100ml or more can compress heart.

of

Heart sounds may be distant, muffled. May have dyspnea or cough. Rapid collection of fluid in pericardial sac; interferes with ventricular filling and pumping; ↓ CO. Caused by pericardial effusion, trauma, cardiac rupture, hemorrhage. Manifestations: Diminished or absent pulse during inspiration (pulsus paradoxus). Drop in systolic BP > 10mmHg during inspiration. Muffled heart sounds ↓Urine output Tachycardia/tachypnea Cool, mottled skin Narrow pulse pressure ↓LOC Distended neck veins (JVD)

Scar tissue formation between pericardial layers eventually contracts, restricting diastolic filling and elevating venous pressures. Manifestations: Progressive dyspnea Fatigue Weakness Ascites common Peripheral edema Neck vein distention during inspiration d/t R atrium being unable to dilate to accommodate ↑ venous return...