Pericardial diseases
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Transcript of Pericardial diseases
1) Anatomy of pericardium2) Overview of pericardial disease3) Clinical presentation4) 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)Infection2)Radiation3)Neoplasm4)Myocardial intrinisic disease5)Trauma6)Autoimmune7)Drugs8)Metabolic
*viral, autoreactive/autoimmune, and neoplastic most common diagnosis
Viral -adenovirus-enterovirus-
cytomegalovirus-influenza-hepatitis B-herpes
simplex-echovirus-mumps
Mycoplasma
Fungal
Parasitic
Bacterial-staphylococcus-streptococcus-pneumococcus-haemophilus-neisseria-chlamydia-legionella-tuberculous-lyme disease
Radiation
Neoplasm-metastatic-primary cardiac-paraneoplastic
Cardiac-early infarction-Dressler’s-myocarditis-aortic dissection
Trauma-blunt-iatrogenic (perforations, post-surg)
Autoimmune-rheumatic disease-non-rheumatic
-Wegners, sarcoid, IBD
Drugs-drug induced lupus
hydralazineisoniazid
procainamide-doxorubicin-phenytoin
Metabolic-hypothyroid-uremia-ovarian hyperstimulation
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 flat2) 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 changes4) 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