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

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