Pericarditis pathophysiology


 * Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S.;

Overview
Pericarditis is inflammation of the pericardium, the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflammed as well. If the myocardium is involved in the inflammatory process, then this is called myopericarditis, and the CK and troponin may be elevated.

Classification
Pericarditis can be classified according to the composition of the inflammatory exudate or the composition of the fluid that accumulates around the heart.

Types include:
 * Serous
 * Purulent
 * Fibrinous
 * Caseous
 * Hemorrhagic
 * Post infarction or Dressler's Syndrome

Acute Versus Chronic Pericarditis
Depending on the timing of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Clinically, acute pericarditis presents within 6 weeks of the disease onset; subacute pericarditis presents within 6 weeks to 6 months of the disease onset; and chronic pericarditis manifests after 6 months of the disease onset.Acute pericarditis is more common than chronic pericarditis, and often occurs as a complication of viral infections, immunologic conditions, or as a result of a heart attack (myocardial infarction). Chronic pericarditis is less common, which may manifest as scarring of the pericardium a condition known as constrictive pericarditis.

Pathogenesis

 * Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may cause pericardial effusion and fibrinous change of pericardium. Most patients with viral pericarditis recover completely with few developing recurrences . Some patients develop constrictive pericarditis which could be disabling.


 * Bacterial pericarditis results from
 * 1) Contiguous spread of infection within the chest, either de novo or after surgery or trauma
 * 2) Spread from infective endocarditis
 * 3) Hematogenous spread of infection
 * 4) Direct inoculation as a result of penetrating injury or cardiothoracic surgery


 * Tuberculous pericarditis develop from lymphatic spread from peritracheal, peribronchial or mediastinal lymphnodes or by contiguous spread from a focus of infection in lung or pleura. There are four pathologic stages observed:


 * Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium


 * Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells


 * Stage 3: Absorption of effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.


 * Stage 4: Development of constrictive pericarditis. Pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue.


 * Pericarditis in renal failure is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins such as urea, creatinine, methylguanidine.

Gross Pathology Images
Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Microscopic Pathology Images
Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Videos
Acute fibrinous pericarditis