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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
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Chapter Summary
This chapter outlines the etiology, clinical presentation, investigation, and management of pericardial effusions and cardiac tamponade (see Fuster and Hurst’s Central Illustration). Pericardial effusions are most commonly idiopathic in etiology in developed countries, while tuberculous pericarditis is the predominant etiology in developing countries. Cardiac tamponade results when intrapericardial pressure elevation impairs cardiac filling with resulting hemodynamic derangements. The rate of pericardial fluid accumulation is a key factor in the development of cardiac tamponade, whereby small volume rapidly accumulating pericardial effusions can result in cardiac tamponade. Clinical evaluation of patients with pericardial effusions should assess for features of cardiac tamponade, including symptoms, tachycardia, hypotension, pulsus paradoxus, and jugular venous pressure elevation. Transthoracic echocardiography is the key diagnostic test in the evaluation of pericardial effusions and assessment of cardiac tamponade, and should be performed in patients with suspected cardiac tamponade. Management of pericardial effusions should target the underlying etiology, with utilization of anti-inflammatory therapy in those with evidence of active pericardial inflammation. Amongst patients with cardiac tamponade, pericardiocentesis is the intervention of choice and should ideally be performed under imaging guidance.
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PERICARDIAL PHYSIOLOGY
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The pericardial cavity arises between the visceral and parietal layers of the serous pericardium (see Fig. 53.1, Chapter 53), typically containing 15 mL to 35 mL of physiologic pericardial fluid. Pericardial fluid, which is produced through ultrafiltration of plasma, provides lubrication between the actively contracting heart beneath it and adjacent surrounding structures. The serous pericardial surface comprises of a single layer of mesothelial cells with numerous microvilli and occasional cilia that protrude into the pericardial space. Tight intracellular junctions between these mesothelial cells, comprising of zona occludens and desomsomal junctions, form a barrier allowing filtration of plasma to create pericardial fluid.1 Pericardial fluid production is a balance between hydrostatic pressure pushing fluid into the pericardial space and osmotic pressure drawing fluid back into the intravascular space, and so alterations in these can result in increases in pericardial fluid volumes. Increased hydrostatic pressures resulting from intravascular volume expansion such as in patients with heart failure; or decreased plasma osmotic pressure resulting from hypoproteinemia in conditions such as cirrhosis and nephrotic syndrome can result in increased pericardial fluid volumes. Pericardial inflammation can result in increased vascular permeability, which also results in pericardial fluid accumulation. Pericardial fluid drainage occurs via the lymphatic system. Distinctive connective tissue structures, with a macroscopic milky spot-like appearance protruding into the pericardial cavity, allow direct communication between the pericardial cavity and lymphatic capillaries allowing drainage of the pericardial fluid via lymphatic vessels.2 Hence damage to lymphatic structures, including particularly the thoracic duct, can result in the formation of chylous pericardial effusions (Fig. 54–1).
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