Pericarditis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby Homa Najafi, M.D.[3]

Pericarditis is inflammation of the pericardium, which is 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 inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

• The pericardium is made up of two layers:^[1][2][3]
  • Fibrous pericardium:
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno–pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium:
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.

• There are two small chambers or sinuses located where the visceral and parietal pericardium are continuous with one another within the pericardial cavity.^[4][5][6]
• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal myocardium ruptured embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax

• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

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  Thoracic portion of the sympathetic trunk.
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  The thymus of a full-time fetus, exposed in situ.

• 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 the pericardium. The pericardium may also develop a serous or hemorrhagic effusion. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling.^[7][8][9]

• Bacterial pericarditis results from:^{[10][11][12][13][14]}

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 develops from lymphatic spread of peritracheal, peribronchial or mediastinal lymph nodes or by contiguous spread from a focus of infection in the lung or pleura. There are four pathologic stages observed:^[15][16][17]

• 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 the organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.

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

These types of granulomatous pericarditis also occur with fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

• 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, uric acid, methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, and others. It may be associated with hemorrhagic or serous effusion.

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

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

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