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In the 16th century, Vesalius first described the anatomy of the pericardium. In 1674, John Mayow gave the earliest account of constrictive pericarditis: “the heart was nearly covered by cartilage, adherent to its interior so that blood could scarcely enter.” Richard Lower in 1689 accurately described tamponade: “a profuse effusion oppresses and inundates the heart. The walls of the heart are so compressed by the fluid circling everywhere, so that the heart cannot dilate sufficiently to receive the blood, then the pulse becomes exceedingly small, thence succeed syncope and death itself.”1 Franz Schuh did the first successful pericadiocentesis in 1840; Churchill performed the first pericardiectomy in the United States in 1929. Claude Beck described his triad of findings in tamponade in 1935. In 1954, Edler demonstrated a pericardial effusion by ultrasound, and in 1971 Spodick described the EKG findings associated with pericarditis.1,2
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The pericardial sac is formed by the visceral and parietal pericardium, which are continuous with one another at the attachment of the great vessels (Figure 18-1). The visceral component is a single mesothelial cell layer with a submesothelium that is invested directly against the myocardium. The visceral pericardium forms the pericardial fluid, an ultrafiltrate of the plasma, normally 20–50 cm3, which is then drained via the parietal pericardium to the thoracic duct. The parietal component is approximately 1 mm thick and formed of three layers: (1) serosa of mesothelium; (2) fibrosa of dense, wavy collagen fibers and interspersed elastic fibers, also containing fibroblasts, mast cells, nerves, blood vessels, and lymphatics; (3) epipericardium of collagen, elastin, and adipose. It is this third layer that forms the ligaments inferiorly to the diaphragm, superiorly to the deep cervical fascia, anteriorly to the manubrium and sternum, and posteriorly to the vertebral column.3–5
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Although there are many recognized functions of the pericardium, its removal or congenital absence is well tolerated except for partial defects that can lead to cardiac herniation. The tensile strength of the pericardium is greater than the myocardium, and it retracts when incised, suggesting that it is under tension. The pericardium maintains the heart in proper position, acts as a barrier to infection, and prevents overdilation of the chambers in response to hypervolemia. It is devoid of impulse-generating capacity, so it does not produce any EKG deflections.5
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Intrapericardial pressure approximates pleural pressure, varying with respiration to aid in venous return and atrial filling. The tension of the pericardium evenly distributes the pericardial fluid against the heart, allowing the pericardial fluid to ...