Normal Pericardial Anatomy and 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 attached by ligaments
to the manubrium sterni, the xiphoid process, the vertebral column,
and the central tendon of the diaphragm. 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 does play 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
Pericardial Pressure and Normal Function
The true pressure in the normal pericardial space is a matter of some controversy. When measured with fluid-filled catheters, pericardial pressure is very similar to intrapleural pressure: from –1
to –2 mm Hg on average, falling to about –5 mm
Hg with normal inspiration. There is considerable evidence, however,
that the pressure in the normal pericardial space is best considered
as a contact force between visceral and parietal pericardium and
therefore is more appropriately measured by specially-designed flat
balloons. When measured in this way, the pericardial pressure is
clearly higher than the intrapleural pressure, although its true
magnitude remains somewhat uncertain. 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. Once this modest reserve is exceeded,
intrapericardial pressure rises significantly. This can occur if
the cardiac volume increases rapidly, for example, due to acute
right ventricular myocardial infarction, or if additional fluid
accumulates. With significant fluid in the pericardial space, fluid-filled catheters
do provide accurate intrapericardial pressure measurements.
The most common clinical manifestation of viral involvement is acute pericarditis. An unidentified virus almost certainly underlies
most cases of acute idiopathic pericarditis. The possibility of
a viral cause is suggested when pericarditis occurs in the absence
of other factors; it is supported by a more than fourfold rise in
serial viral antibody titers during the initial weeks of illness.
(Such measurement, however, is not a routine part of the management
of viral pericarditis.) Frequently, a prodromal syndrome consistent
with a viral infection is present.
The viral pathogens most commonly associated with pericarditis include coxsackievirus B (most common), coxsackievirus A, echovirus 8, and HIV. Although a wide range of viral agents have been implicated,
no specific antiviral therapy has been shown to be effective; management
and outcome are described in the section on acute pericarditis.
Bacterial infection of the pericardium can occur following thoracic surgery, as a result of a contiguous pleural, mediastinal, or pulmonary infection, as a complication of bacterial endocarditis, or as a
result of systemic bacteremia. Direct extension from pneumonia or
empyema with staphylococci, pneumococci, and streptococci accounts for
most cases. The incidence of hospital-acquired penicillin-resistant
staphylococcal pericarditis after thoracic surgery has increased
during the past decade. Preexisting pericardial effusions and immunosuppressed
states are important predisposing factors.
Common clinical manifestations include fever, chills, night sweats, and dyspnea; pleuritic chest pain and pericardial friction rubs
are present in only a minority of patients. Leukocytosis with a shift to the left is generally present, and chest radiography usually reveals an increase in the cardiac silhouette. Although electrocardiograms (ECGs) are frequently normal, they can show typical changes of acute pericarditis.
Although high intrapericardial antibiotic levels are achievable, medical therapy alone is usually insufficient, and prompt percutaneous or surgical drainage is essential. Cardiac tamponade may occur very
rapidly with hemodynamic deterioration that can be confused with
septic shock. In view of the continuing high mortality rates of
65–77%, bacterial pericarditis should be considered
a medical emergency.
Although several decades of effective antituberculous therapy and public health measures have brought about a declining rate of tuberculous pericarditis, this condition remains a major problem in immunocompromised
persons and in the non-industrialized world. Thus, HIV-associated tuberculosis
is a common cause of symptomatic pericardial effusion.
Tuberculous pericarditis typically occurs with no demonstrable pulmonary or extrapulmonary tuberculosis. Symptoms may be insidious
and nonspecific. Findings are predominantly systemic, and pericardial
friction rubs are unusual. Large effusions (Figure
17–1) and resulting tamponade are common, and constriction
occurs as a late complication. Demonstration of tubercle bacillus
by stain or culture is possible in only one-third to one-half of
the patients, and the diagnosis is often presumptively established
through a history of contact or a positive purified protein derivative (PPD)
skin test. Alternatively, finding characteristic granulomata on
pericardial biopsy specimens confirms the diagnosis, but even these
are often falsely negative. High levels of adenosine deaminase (ADA), an enzyme produced by white blood cells in pericardial fluid, is a sensitive and specific test for tuberculous pericarditis. Increased
interferon-gamma in pericardial fluid is an additional marker. Combined with ADA it provides even greater diagnostic accuracy. Most recently,
polymerase chain reaction (PCR) to detect Mycobacterium
tuberculosis DNA has been used and can be performed in
minute amounts of pericardial fluid. Use of one or more of these