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Pericardial diseases
1.
2.
3. 1) Anatomy of pericardium
2) Overview of pericardial disease
3) Clinical presentation
4) Acute pericarditis
5) Chronic pericarditis
4. Normal amount of
pericardial fluid: 15-50
cc
Two layers:
Outer layer is the parietal
pericardium and consists
of layers of fibrous and
serous tissue
Inner layer is visceral
pericardium and consists
of serous tissue only
5. Fibroelastic sac
consisting of 2 layers
Visceral at
epicardial side
Parietal at
mediastinal side
Pericardial fluid
formed from
ultrafiltrate of plasma
15. Fibrin strands
Inflammatory exudate
Congested capillaries
Exudate can
completely resolve or
can organize leaving
delicate, stringy
adhesions or plaque
like thickening.
16. Usually signifies
bacterial, fungal or
parasitic infection
Direct extension,
hematogenous or
lymphatic spread.
Common organisms
streptococci,
staphylococci and
pneumococci
17. 400- 500 ml
Thin to creamy pus
Erythematous,
granular surface
Can produce
constrictive
pericarditis
18. Exudate of blood
admixed with
fibrinous to
supparative effusion
Most commonly it
follows cardiac
surgery or associated
with tuberculosis or
malignancy
It organize with or
without calcification
19. Due to tuberculosis
Typically by direct
extension from
neighboring lymph
nodes or less
commonly mycotic
infection
Lead to fibro calcific
constrictive
pericarditis.
22. Clinically significant
Pericardial sac obliterated
Parietal layer is tethered to medistinal tissue
Heart so contract against the surrounding
attached structures with hypertrophy and
dilatation.
23. Clinically significant
Thick dense fibrous obliteration with
calcification of the pericardial sac encasing the
heart limiting diastolic expansion and
restricting cardiac output.
24. Normal in
patients with
acute pericarditis
unless
pericardial
effusion is
present
Requires 200cc of
fluid
25.
26. the historic yield of diagnostic evaluation is
low, typically only in 16% of patients is
etiology determined.
evaluation of pericardial fluid and tissue with
tumor markers, PCR, immunohistochemistry,
flourescence-activated cell sorting has shown a
trend toward higher yield of diagnosis
27. 1) Chest pain
Sudden onset
localized to anterior chest wall
pleuritic
sharp
Positional: may improve if pt leans forward, worse
with lying flat
2) Cardiac auscultation: Pericardial friction rub
Present in up to 85% of pts with pericarditis without
effusion
friction of the two inflamed layers of pericardium,
typically triphasic rub, heard with diaphragm of
stethoscope at left sternal border
3) Characteristic ECG changes
4) Pericardial effusion
28. Elevated C reactive protein level
strong correlation - normal CRP makes acute
pericarditis diagnosis less likely
Elevated CK, CK-MB, and Troponin
Often elevated Troponin alone
Indicates inflammation of myocardium just
beneath the visceral pericardium
Not associated with worse outcomes
Leukocytosis
29. 51yo man with acute onset sharp substernal chest pain
two days prior
33. Pressure in pericardium exceeds pressure in
the cardiac chambers, lower chamber atria
affected before higher pressure ventricles
Compressive effect is seen best in the phase
when the intrachamber pressure is lowest –
systole for atria and diastole for ventricles
Diagnostic techniques
2D looking for RA/RV collapse during diastole
M-mode for RA/RV collapse during diastole
Doppler of Mitral and Tricuspid inflow
Mitral inflow to decrease by 25% with inspiration
Tricuspid inflow increased by 40% with inspiration
IVC diameter fails to increase with inspiration