Cardiac Valvular Disease 3 Flashcards

1
Q

bacterial or fungal infection of valves or endocardium including great vessels

A

infective endocarditis

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2
Q

IE risk factors NATIVE valve

A
  1. rheumatic, congenital or degenerative valve disease
  2. congenital heart disease
  3. IVDA
  4. HACIE (health care cause)
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3
Q

native IE pathophysiology

A

bacteria or fungi gain access to the valve during transient bacteremia

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4
Q

what might cause transient bacteremia

A
chronic wound 
dental procedure 
IVDA 
central line 
UTI, pneumonia
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5
Q

why are those with cardiac valve abnormalities predisposed to IE

A

altered hemodynamics, creates areas with stasis with bacterial flow

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6
Q

average age of patient with IE? why?

A

OLDER

decreased rheumatic disease, increased degenerative disease

increased instrumentation, invasive procedures, lines predisposing pt

people living longer immunosuppression

significant # IE, nosocomial now

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7
Q

underlying diseases in IE

A
Atherosclerotic 
MVP 
Congenital 
PVE 
Rheumatic
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8
Q

valves mc affected?

A

MITRAL

aortic, mitral and aortic, tricuspid

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9
Q

native valve organisms

A
staphylococcus aureus 
streptococcus viridans 
group D streptococcus 
Enterococci 
HAECK
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10
Q

natural history of IE due to
rapid valvular destruction

organisms

A

CHF also

s. aureus
strep pneumoniae
strep pyogenes
neisseria gonorrhea

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11
Q

natural history of IE due to

indolent valvular destruction

A

few symptoms

strep viridians
enterococcus faecalis
GNRs

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12
Q

prosthetic valve replacement and IE

early IE

A

within 60 days

contamination in surgery or hematogenous seeding from extra cardiac site

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13
Q

prosthetic valve replacement and IE

late IE

A

oral site that seeds valve

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14
Q

IVDA and IE

A

majority don’t have known valve dz

more likely to affect tricuspid valve

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15
Q

tricuspid valve and IVDA IE

A

injection of drugs directly into vein (first stop)

drugs cut with TELK cause small bits of damage over the course of time

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16
Q

what organisms in IVDA IE?

A

s. aureus
pseudomonas
unusual pathogens
polymicrobial

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17
Q

vegetation

A

mass of fibrin and cellular elements of blood that become haven for bacterial growth

found @ sites of congenital malformation or areas of valve damage on L side of heart

low pressure side of valve

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18
Q

Pathology of IE

A

infection in blood and vegetation formation causes bacterial proliferation and destruction on valve

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19
Q

why low pressure

A

easier growth due to less rapid blood flow movement

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20
Q

IE on which lesions

A

small, tight lesions

high pressure differential also promotes

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21
Q

clinical IE presentation

A

Fever (MC)

heart murmur

embolic phenomena

clubbing

general illness symptoms

** timing can clue us into which pathogen

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22
Q

Classic symptoms of IE

A

splinter hemorrhages

petechiae

roth spots

janeway lesions

osler nodes

23
Q

roth spots

A

exudative, edematous hemorrhagic retinal lesions

24
Q

subungual, vertical lines

A

splinter hemorrhages

25
Q

laneway lesions

A

PAINLESS

macules or nodular

hemorrhages on palms and soles

microabsecess with neutrophil invasion

26
Q

osler nodes

A

PAINFUL

raised lesions

occur in crops on tips of fingers and toes or on hands/feet

transient

27
Q

IE diagnostic studies

A

TEE (check for vegetations)

Blood culture (multiple sets, q 15 min x 3 sets)

28
Q

diagnostic studies in IE other

A

CXR

EKG

CBC, BMP, additional labs

29
Q

duke criteria IE

A

2 major, 1 major/3 minor or 5 minor

30
Q

Major diagnostic criteria

A
  1. positive blood culture for typical infective endocarditis
  2. new regurgitant murmur or echo findings consistent with IE
31
Q

IE complications (6)

A
  1. cardiac valve destruction
  2. metastatic infection (i.e. kidney, head, spleen, liver, lung)
  3. embolization
  4. Myocardial abscess
  5. conduction derangement
  6. immune mediated effects
32
Q

IE treatment

A

hospitalize

empiric abx after blood culture drawn

following identification, narrow/targeted abx treament

ID involvement

33
Q

empiric abx IE

A

gram +, gram -

+/- fungal or anaerobic coverage

Rocephin and vancomycin

34
Q

when might we consider fungal cause of IE?

A

IMMUNOSUPPRESED

HIV, taking immunosuppresive meds, transplant patient, SLE, cancer, asplenia

35
Q

targeted IE tx

staph aureus

A

MSSA: naficillin IV x 6+ wks

MRSA: vancomycin IV x6+wks

36
Q

targeted IE tx

enterococcus

A

ampicillin
entamycin
daptomycin

37
Q

targeted IE tx

strep

A

aq PCN V iv x4+ weeks

38
Q

indications for surgical IE tx

A

acute HF (unresponsive to abx)

infections unresponsive to meds

abscess formation, recurrent emoli

recurrent infection

39
Q

what to look for if IE symptoms persist?

A

another pathogen?

incorrect pathogen?

giving right Abx?

get new blood cultures, CT/MRI

40
Q

IE prophylaxis for who? what do we give + dose?

A

considered for patients that have high risk cardiac conditions and getting a high risk procedure

amox 2mg po 1 hr prior

41
Q

who DOES not get IE prophylaxis

A

Rheumatic heart disease: MVP +/- MR, bicuspid aortic valve, HOCM, ASD

h/o pacers, stents, ICD, CABG

42
Q

two layer sac around heart

A

pericardium

43
Q

normal amount of pericardial fluid

A

5-15mL

provides lubrication between heart and surrounding viscera

44
Q

diseases of pericardium

A

acute pericarditis

pericardial effusion

chronic pericarditis

45
Q

inflammation of sac surrounding heart

A

acute pericarditis

46
Q

collection of inflammatory fluid that forms between visceral and partial pericardial layers

A

pericardial effusion

47
Q

permanent scarring of pericardium secondary to inflammation

A

chronic pericarditis

48
Q

etiologies of acute pericarditis

A
  1. viral
  2. TB
  3. Uremia (renal failure)
  4. neoplastic syndrome
  5. inflammatory (dresser’s or connective tissue disorder)
49
Q

symptoms of acute pericarditis

A

Chest pain

dyspnea

fever

50
Q

Chest pain in acute pericarditis

A

sharp, sub sterna CP begins abruptly and non pleuritic

exacerbated by lying down

received when sitting up and leaning forward

51
Q

sings of acute pericarditis

A

Friction rub

s.s of altered hemodynamics

EKG changes (saggy ST w.o. reciprocal changes)

52
Q

diagnostic studies

A

echocardiography

CBC + chemistries
Cardiac markers
ESR + CRP
TSH/ANA/PPD

53
Q

idiopathic tx of acute pericarditis

A

NSAIDS to relieve inflammation and pain

colchicine (90 days)

+/- oral corticosteroids and pericardial window