Normal Pericardial Anatomy & Physiology
The pericardium consists of two layers: a serous visceral layer, which is intimately adherent to the heart and epicardial fat, and a fibrous parietal layer. The pericardium encloses the greater part of the surface of the heart, the juxtacardial portions of the pulmonary and systemic veins, and the proximal segments of the great vessels. A significant portion of the left atrium, however, is not enclosed within the pericardium. The pericardium is not essential for sustaining life or health, as evidenced by preservation of cardiac function even if the pericardium is congenitally absent or surgically removed. The pericardium plays a role in normal cardiovascular function, however, and can be involved in a number of important disease states. The normal functions of the pericardium include maintaining an optimal cardiac shape, promoting cardiac chamber interaction, preventing the overfilling of the heart, reducing friction between the beating heart and adjacent structures, providing a physical barrier to infection, and limiting displacement during the cardiac cycle.
Pericardial Pressure & Normal Function
The bulk of current evidence indicates that with normal cardiac volumes, the effective pericardial pressure ranges from 0–1 mm Hg to (at most) 3–4 mm Hg. The pericardial space between the parietal and visceral layers normally contains 15–50 mL of fluid, and the reserve volume of the pericardium is relatively small. The pericardium has a limited distensibility essentially determined by the histologic composition of the parietal pericardium with a limited amount of elastic fibers and more collagen fibers. However, if pericardial fluid accumulates slowly, a remodeling of pericardial connective tissue may allow pericardial distension with accumulation of 1000–1500 mL of fluid, and occasionally up to 2000 mL. Normally, acute tamponade occurs with accumulation of < 250 mL. The pressure–volume relation of normal pericardium is a J-shaped curve. After an initial short shallow portion, which allows the pericardium to prevent cardiac chamber dilatation in response to physiologic events such as posture changes, there is a minimal increase in pericardial pressure. Thereafter, the pressure increase is extremely steep for sudden, acute changes of volume. Thus, an acute increase of 100–200 mL may greatly elevate pericardial pressure to 20–30 mm Hg and be responsible for cardiac tamponade. On the contrary, a slowly increasing pericardial volume is accompanied by only modest increase of pericardial pressure until 1000–2000 mL before the development of cardiac tamponade.
Pericardial diseases are relatively common in clinical practice and may have different presentations either as isolated disease or manifestation of a systemic disorder. Although the etiology is varied and complex (Table 28–1), the pericardium has a relatively nonspecific response to these different causes. On this basis, there are few main clinical presentations including pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis. Causes are essentially divided as infectious or noninfectious.
Table 28–1. Etiology of Pericardial Diseases |Favorite Table|Download (.pdf)
Table 28–1. Etiology of Pericardial Diseases
Viral (coxsackievirus, influenza, Epstein-Barr virus, cytomegalovirus, adenovirus, varicella, rubella, mumps, hepatitis B virus, hepatitis C virus, HIV, parvovirus B19, and human herpes virus 6)
Bacterial (tuberculosis, Coxiella burnetii, other bacterial rare may include pneumo-, meningo-, gonococcosis, Haemophilus, streptococci, staphylococci, Chlamydia, Mycoplasma, Legionella, Leptospira, Listeria)
Fungal (rare: Histoplasma more likely in immunocompetent patients; aspergillosis, blastomycosis, Candida more likely in immunosuppressed host)
Parasitic (very rare: Echinococcus, Toxoplasma)
Pericardial injury syndromes (postmyocardial infarction syndrome, postpericardiotomy syndrome, posttraumatic ...
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