Endocarditis & Cardiac Infections Flashcards by Kyra Porter

layers lining the heart (from outermost to innermost)

pericardium (outermost layer): composed of:
-fibrous pericardium
-serous pericardium (parietal layer)
-pericardial space
-serous pericardium (visceral layer; aka epicardium)
myocardium (muscle layer)
endocardium (inner endothelial lining covering trabeculae)

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pericarditis - overview

*inflammation of the lining around the heart (pericardium)

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pericarditis - etiologies

*often idiopathic
*VIRAL INFECTIONS (coxsackie B
*other infectious causes (bacteria, fungi, parasites)
*malignancy
*cardiac surgery
*thoracic radiotherapy (early)
*MI (postcardiac injury syndrome)
*autoimmune diseases (SLE, rheumatoid arthritis)
*renal failure (uremia)

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pericarditis - clinical presentation

*sharp chest pain
-aggravated by inspiration
-relieved by sitting up & LEANING FORWARD
*PERICARDIAC FRICTION RUB on auscultation
*can be complicated by a pericardial effusion
*classic presentation: YOUNG ADULT, usually male, with CHEST PAIN

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pericarditis - diagnosis

*diagnosed by physical exam, echocardiogram, EKG, and pericardiocentesis (if pericardial effusion):

-PE: sharp chest pain, pericardial friction rub
-echo:
-EKG: widespread/diffuse ST-segment elevation and/or PR depression

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pericarditis - treatment

*anti-inflammatories if viral (NSAIDs, colchicine)
*antibiotics if bacterial

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myocarditis - overview

*inflammation of the heart muscle itself (inflammation of myocardium)
*major cause of sudden cardiac death in adults < 40 yo

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myocarditis - etiologies

*VIRAL (coxsackie B, echoviruses)
*parasitic
*bacterial
*toxins
*rheumatic fever
*drugs
*autoimmune

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myocarditis - clinical presentation

*highly variable
*classically presents in younger adults
*heart failure signs predominant (dyspnea, pulmonary edema, peripheral edema, dyspnea on exertion)
*fever, dyspnea, chest pain, arrythmias *persistent tachycardia out of proportion to fever

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myocarditis - diagnosis

*echocardiogram: low EF, decreased heart wall movements
*serologies for likely causes
*possibly biopsy

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myocarditis - treatment

*supportive, using anti-inflammatories

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COVID-19 myocarditis

*virus binds its spike to membrane ACE2 (found in higher concentrations on male > female cells)
*combination of direct myocardial cell infection & damage from inflammatory response
*estimated that COVID has > 15-fold risk of myocarditis compared to other viruses
*vaccine was also implicated
*can cause life-threatening arrhythmias

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infective endocarditis (IE) - overview

*infection of the lining membranes of the heart or its valves
*usually caused by a BACTERIAL infection

*most commonly infects sites of pre-existing lesions (rheumatic heart disease, unrepaired congenital heart disease, mitral valve prolapse, etc)
*associated with IV DRUG USE
*increasing incidence of healthcare-associated IE (dialysis patients, central lines, cardiac devices, prosthetic valves)

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infective endocarditis (IE) - right vs. left side heart valve disease

*in non-drug users, left-sided disease dominates (mitral valve, aortic valve)

*IV drug use:
-mean age ~30 yo
-RIGHT-sided tricuspid valve disease much more common & considered a hallmark
-note: can have left-sided valve disease as well

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infective endocarditis (IE) - etiologies (pre-antibiotic era)

*viridans streptococci predominate
*rheumatic heart disease is key risk factor
*subacute processes key to diagnoses:
-glomerulonephritis
-splenomegaly
-Osler’s nodes and roth spots

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infective endocarditis (IE) - etiologies (in US)

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*STAPH AUREUS predominates, causing a rapid/acute disease course
-median age > 50yo
*risk factors include: IVDU, CIEDs, prosthetic valves
*diagnosis: modified Duke Criteria

infective endocarditis (IE) - pathophysiology

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damaged endothelium exposes collagen & matrix molecules
platelets & fibrin adhere to these exposed molecules → sterile vegetation forms (nonbacterial thrombotic endocarditis)
circulating bacteria seed this vegetation following a transient bacteremia
lots of bacteria densely pack in to vegetation:
-keep bacteria in circulation
-circulating bacteria continue to feed the thrombus
-more platelets and fibrin deposit
-growing, increasingly friable thrombus develops
developing complications: ring abscess, myocarditis, and vegetation emboli

infective endocarditis (IE) - pathophysiology of vegetation

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*only certain bacteria or strains of bacteria have virulence factors that allow them to attach and infect the endothelium/sterile vegetations

*the vegetation is building progressive layers around the core:
-quorum sensing in the core: gene expression alterations in areas of high bacteria density; allows simultaneous upregulation of genes for virulence factors & more
-BIOFILMS: bacteria which stick to each other & a surface and coat themselves in a difficult-to-penetrate extracellular matric

most common cause of infective endocarditis

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STAPH AUREUS > streptococci

infective endocarditis (IE) - modified duke criteria (MAJOR criteria)

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valve culture/histopathology (during heart surgery)
blood culture criteria: 2 blood cultures with typical organisms (Staph aureus, viridans strep, etc)
echo criteria:
-vegetation or abscess
-prosthetic valve dehiscence
-new valvular regurgitation

infective endocarditis (IE) - modified duke criteria (MINOR criteria)

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predisposing heart condition or IVDU
fever > 100.4
embolic phenomena (vegetation broke off and traveled to another organ, including brain)
immunologic phenomena (immune complex deposition, glomerulonephritis, Roth spots)
blood culture not meeting major criteria

infective endocarditis (IE) - Osler’s Node

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*example of an immunologic phenomenon seen in infective endocarditis
*PAINFUL, RAISED, violaceous lesions on finger or toe pads
*immune-mediated vasculitis

infective endocarditis (IE) - Janeway Lesions

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*example of an embolic phenomenon seen in infective endocarditis
*macules
*micro abscesses with neutrophil infiltration of capillaries (septic emboli to skin)

infective endocarditis (IE) - Roth Spots

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*example of an immunologic phenomenon seen in infective endocarditis
*retinal hemorrhagic lesions with central clearing (pale centers)
*can be seen in other conditions

infective endocarditis (IE) - Duke Scoring

*definite endocarditis: 2 major criteria OR 1 major + 3 minor OR 5 minor OR positive culture from tissue OR coxiella anti-phase 1 IgG titer > 1:800 *possible endocarditis: 1 major criteria + 1-2 minor OR 3 minor *rejected endocarditis: firm alternative diagnosis OR resolution of manifestations after antibiotic therapy for 4 days OR no pathological evidence at surgery or on autopsy

infective endocarditis (IE) echocardiogram principles (when to perform transthoracic vs transesophageal)

*transesophageal (TEE) is better if there is vegetation on a prosthetic valve or an abscess *transthoracic (TTE) is generally sufficient for a right-sided infective endocarditis *if high concern, do a TEE *if see IE or TTE, and there are concerns for complications, then do a TEE

infective endocarditis (IE) - antibiotic treatment principles

*static organisms in stasis at the center of the vegetation *antibiotic penetration: -vancomycin: concentrates on periphery and has poor penetration inward -beta lactams: do perfuse inward, but with steep concentration gradient -homogenous diffusion through the whole lesions: tobramycin, fluoroquinolones, daptomycin *CIDAL > STATIC, MAX OUT THE DOSES

infective endocarditis (IE) - antibiotic regimen

*at least 10 days of IV antibiotics, followed by long-term oral antibiotics course *make sure that the antibiotics you choose cover the infectious organism

causes of culture-negative endocarditis

*candida *coxiella *bartonella *chlamydia species *brucella *legionella *fungi *acid-fast bacilli

dental prophylaxis for infective endocarditis

*people with risk factors sometimes now receive prophylactic antibiotics prior to dental procedures to prevent development of endocarditis (usually amoxicillin) *guidelines restrict the prophylaxis to those with: -previous IE -prosthetic heart valve or prosthetic material used for heart repair -UNREPAIRED cyanotic heart disease -completely repaired congenital heart disease in 6 months post-surgery -congenital heart disease with residual deficits -cardiac transplant patient with valvuloplasty

rheumatic fever & heart disease - epidemiology

*mostly in age 5-14 years old *pretty common *acute rheumatic fever leading to rheumatic heart disease: 2 to 3 weeks after group A strep throat infection (or occasionally skin infections)

acute rheumatic fever - J❤️NES Criteria

*JOINTS: large joint arthritis/arthralgia *❤️ (heart): rheumatic carditis with inflammation of cardiac tissue, especially the mitral and aortic valves & heart walls *NODULES: subcutaneous nodules (hard and painless on extensor surfaces) *Erythema marginatum (evanescent rash with ring margin) *Sydenham chorea (involuntary irregular movements of limbs and face)

rheumatic heart disease - pathophysiology

*carditis: molecular mimicry -strep M protein & other antigens cause cross-reaction for nervous system and heart tissue -Aschoff bodies: intense inflammation in the heart leads to nodules of T cells and macrophages -inflammation causes valve leaflets to fuse together, chordae to shorten, and rigidity *rheumatic heart disease: chronic heart disease due to persistent damage to heart valve from the immune response & repeat infections -MITRAL VALVE most commonly affected (classically, MITRAL STENOSIS)

rheumatic heart disease - prevention & treatment

*prevented by penicillin treatment of strep throat *if develop rheumatic fever, need ongoing penicillin to prevent recurrent acute rheumatic fever and worsening rheumatic heart disease

aortitis - overview & symptoms

*inflammation of aorta itself; seeding of an atherosclerotic plaque or aneurysm sac by vaso vasorum *symptoms: vary; back pain, fever, dissection

aortitis - etiologies

*non-typhoidal Salmonella *SYPHILIS *staphylococcus & strep pneumo *TB

aortitis - diagnosis & treatment

*dx: CTA or MR angiogram *tx: ? antibiotics & surgical management

Lemierre's Syndrome

*infectious thrombophlebitis of internal jugular *classically presents in young & healthy patients with prolonged tonsillitis, progressing to sepsis; septic emboli to lung is common *FUSOBACTERIUM NECROPHORUM most common pathogen *tx with antibiotics usually

CIED infections

*infections of cardiac IEDs, at time of implantation or through bacteriemia *s/s: local inflammation/erythema or erosion at pocket, bacteremia, FUO *organisms: CoNS, S. aureus, gram negatives *dx: TEE, blood cultures, culture of pocket/leads *tx: ICR removal and 2-6 weeks of antibiotics like IE treatment

Endocarditis & Cardiac Infections Flashcards

(39 cards)