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1) Anatomy of pericardium

2) Overview of pericardial disease


3) Clinical presentation
4) Acute pericarditis
5) Chronic pericarditis
 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
 Fibroelastic sac
consisting of 2 layers
 Visceral at
epicardial side
 Parietal at
mediastinal side
 Pericardial fluid
formed from
ultrafiltrate of plasma
 Acute Pericarditis
 Chronis pericarditis
 Pericardial Effusion
1)Infection
2)Radiation
3)Neoplasm
4)Myocardial intrinisic disease
5)Trauma
6)Autoimmune
7)Drugs
8)Metabolic

*viral, autoreactive/autoimmune, and neoplastic most


common diagnosis
Viral Fungal
-adenovirus
-enterovirus Parasitic
-cytomegalovirus Bacterial
-influenza -staphylococcus
-hepatitis B -streptococcus
-herpes simplex -pneumococcus
-echovirus -haemophilus
-mumps -neisseria
-chlamydia
Mycoplasma -legionella
-tuberculous
-lyme disease
Radiation Trauma
-blunt
Neoplasm -iatrogenic (perforations, post-
-metastatic surg)
-primary cardiac
-paraneoplastic Autoimmune
-rheumatic disease
Cardiac -non-rheumatic
-early infarction -Wegners, sarcoid, IBD
-Dressler’s
-myocarditis
-aortic dissection
Drugs Metabolic
-drug induced lupus -hypothyroid
hydralazine -uremia
isoniazid -ovarian
procainamide hyperstimulation
-doxorubicin
-phenytoin
 Serous
 Fibrinous
 Purelent
 Hemorrahgic
 Caseous
 50-200ml exudate
 Etiology unknown
 Scant acute and ch
inflammatory
infiltrate

 Fluid reabsorb leaving


any residual change
 Most commonly seen
in MI
 Associated with
friction rub
 Fibrin strands
 Inflammatory exudate
 Congested capillaries
 Exudate can
completely resolve or
can organize leaving
delicate, stringy
adhesions or plaque
like thickening.
 Usually signifies
bacterial, fungal or
parasitic infection
 Direct extension,
hematogenous or
lymphatic spread.
 Common organisms
streptococci,
staphylococci and
pneumococci
 400- 500 ml
 Thin to creamy pus
 Erythematous,
granular surface
 Can produce
constrictive
pericarditis
 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
 Due to tuberculosis
 Typically by direct
extension from
neighboring lymph
nodes or less
commonly mycotic
infection
 Lead to fibro calcific
constrictive
pericarditis.
 Central caseous
necrosis
 Epitheliod histiocytes
forming granulomas
 Giant cells.
 Healing of acute lesions

 Adhesive medistinopericarditis
 Constrictive pericarditis
 Clinically significant
 Pericardial sac obliterated
 Parietal layer is tethered to medistinal tissue
 Heart so contract against the surrounding
attached structures with hypertrophy and
dilatation.
 Clinically significant
 Thick dense fibrous obliteration with
calcification of the pericardial sac encasing the
heart limiting diastolic expansion and
restricting cardiac output.
 Normal in
patients with
acute pericarditis
unless
pericardial
effusion is
present
 Requires 200cc of
fluid
 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
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
 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
 51yo man with acute onset sharp substernal chest pain
two days prior
 Low voltage and Electric Alternans
 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
 www.bidmc.org
 www.heartydog.co.uk
 www.budjzdorov.org.ua
 www.histopathology-india.net

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