Cardiac Valvular Disease 3 Flashcards
bacterial or fungal infection of valves or endocardium including great vessels
infective endocarditis
IE risk factors NATIVE valve
- rheumatic, congenital or degenerative valve disease
- congenital heart disease
- IVDA
- HACIE (health care cause)
native IE pathophysiology
bacteria or fungi gain access to the valve during transient bacteremia
what might cause transient bacteremia
chronic wound dental procedure IVDA central line UTI, pneumonia
why are those with cardiac valve abnormalities predisposed to IE
altered hemodynamics, creates areas with stasis with bacterial flow
average age of patient with IE? why?
OLDER
decreased rheumatic disease, increased degenerative disease
increased instrumentation, invasive procedures, lines predisposing pt
people living longer immunosuppression
significant # IE, nosocomial now
underlying diseases in IE
Atherosclerotic MVP Congenital PVE Rheumatic
valves mc affected?
MITRAL
aortic, mitral and aortic, tricuspid
native valve organisms
staphylococcus aureus streptococcus viridans group D streptococcus Enterococci HAECK
natural history of IE due to
rapid valvular destruction
organisms
CHF also
s. aureus
strep pneumoniae
strep pyogenes
neisseria gonorrhea
natural history of IE due to
indolent valvular destruction
few symptoms
strep viridians
enterococcus faecalis
GNRs
prosthetic valve replacement and IE
early IE
within 60 days
contamination in surgery or hematogenous seeding from extra cardiac site
prosthetic valve replacement and IE
late IE
oral site that seeds valve
IVDA and IE
majority don’t have known valve dz
more likely to affect tricuspid valve
tricuspid valve and IVDA IE
injection of drugs directly into vein (first stop)
drugs cut with TELK cause small bits of damage over the course of time
what organisms in IVDA IE?
s. aureus
pseudomonas
unusual pathogens
polymicrobial
vegetation
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
Pathology of IE
infection in blood and vegetation formation causes bacterial proliferation and destruction on valve
why low pressure
easier growth due to less rapid blood flow movement
IE on which lesions
small, tight lesions
high pressure differential also promotes
clinical IE presentation
Fever (MC)
heart murmur
embolic phenomena
clubbing
general illness symptoms
** timing can clue us into which pathogen
Classic symptoms of IE
splinter hemorrhages
petechiae
roth spots
janeway lesions
osler nodes
roth spots
exudative, edematous hemorrhagic retinal lesions
subungual, vertical lines
splinter hemorrhages
laneway lesions
PAINLESS
macules or nodular
hemorrhages on palms and soles
microabsecess with neutrophil invasion
osler nodes
PAINFUL
raised lesions
occur in crops on tips of fingers and toes or on hands/feet
transient
IE diagnostic studies
TEE (check for vegetations)
Blood culture (multiple sets, q 15 min x 3 sets)
diagnostic studies in IE other
CXR
EKG
CBC, BMP, additional labs
duke criteria IE
2 major, 1 major/3 minor or 5 minor
Major diagnostic criteria
- positive blood culture for typical infective endocarditis
- new regurgitant murmur or echo findings consistent with IE
IE complications (6)
- cardiac valve destruction
- metastatic infection (i.e. kidney, head, spleen, liver, lung)
- embolization
- Myocardial abscess
- conduction derangement
- immune mediated effects
IE treatment
hospitalize
empiric abx after blood culture drawn
following identification, narrow/targeted abx treament
ID involvement
empiric abx IE
gram +, gram -
+/- fungal or anaerobic coverage
Rocephin and vancomycin
when might we consider fungal cause of IE?
IMMUNOSUPPRESED
HIV, taking immunosuppresive meds, transplant patient, SLE, cancer, asplenia
targeted IE tx
staph aureus
MSSA: naficillin IV x 6+ wks
MRSA: vancomycin IV x6+wks
targeted IE tx
enterococcus
ampicillin
entamycin
daptomycin
targeted IE tx
strep
aq PCN V iv x4+ weeks
indications for surgical IE tx
acute HF (unresponsive to abx)
infections unresponsive to meds
abscess formation, recurrent emoli
recurrent infection
what to look for if IE symptoms persist?
another pathogen?
incorrect pathogen?
giving right Abx?
get new blood cultures, CT/MRI
IE prophylaxis for who? what do we give + dose?
considered for patients that have high risk cardiac conditions and getting a high risk procedure
amox 2mg po 1 hr prior
who DOES not get IE prophylaxis
Rheumatic heart disease: MVP +/- MR, bicuspid aortic valve, HOCM, ASD
h/o pacers, stents, ICD, CABG
two layer sac around heart
pericardium
normal amount of pericardial fluid
5-15mL
provides lubrication between heart and surrounding viscera
diseases of pericardium
acute pericarditis
pericardial effusion
chronic pericarditis
inflammation of sac surrounding heart
acute pericarditis
collection of inflammatory fluid that forms between visceral and partial pericardial layers
pericardial effusion
permanent scarring of pericardium secondary to inflammation
chronic pericarditis
etiologies of acute pericarditis
- viral
- TB
- Uremia (renal failure)
- neoplastic syndrome
- inflammatory (dresser’s or connective tissue disorder)
symptoms of acute pericarditis
Chest pain
dyspnea
fever
Chest pain in acute pericarditis
sharp, sub sterna CP begins abruptly and non pleuritic
exacerbated by lying down
received when sitting up and leaning forward
sings of acute pericarditis
Friction rub
s.s of altered hemodynamics
EKG changes (saggy ST w.o. reciprocal changes)
diagnostic studies
echocardiography
CBC + chemistries
Cardiac markers
ESR + CRP
TSH/ANA/PPD
idiopathic tx of acute pericarditis
NSAIDS to relieve inflammation and pain
colchicine (90 days)
+/- oral corticosteroids and pericardial window
