Pain is often absent in

slowly developing tuberculous, postirradiation, and neoplastic,

uremic, and constrictive pericarditis.
The base of the left lung may be compressed
by pericardial fluid, producing Ewart’s sign, a patch of dullness
and increased fremitus (and egophony) beneath the angle of
the left scapula. The chest roentgenogram may show enlargement
of the cardiac silhouette, with a “water bottle” configuration, but
may be normal.
Viral or idiopathic acute pericarditis occurs at all ages but is more
common in young adults and is often associated with pleural effusions
and pneumonitis. The almost simultaneous development of fever and
precordial pain, often 10–12 days after a presumed viral illness, constitutes
an important feature in the differentiation of acute pericarditis
from AMI, in which chest pain precedes fever. The constitutional
symptoms are usually mild to moderate, and a pericardial friction rub
is often audible. The disease ordinarily runs its course in a few days to
4 weeks. The ST-segment alterations in the ECG usually disappear
after 1 or more weeks, but the abnormal T waves may persist for
several years and be a source of confusion in persons without a clear
history of pericarditis. Pleuritis and pneumonitis frequently accompany
viral or idiopathic acute pericarditis
The diagnosis of pericardial fluid or thickening may be confirmed 1573
by computed tomography (CT) or magnetic resonance imaging
(MRI). These techniques may be superior to echocardiography in
detecting loculated pericardial effusions, pericardial thickening, and
the identification of pericardial masses.
ASA is suggested in patients with post-MI pericarditis or Dressler syndrome
as
other NSAIDs are contraindicated in the setting of an acute MI.
Glucocorticosteroids and NSAIDs are avoided after an MI due to a risk
forimpaired ventricular healing, which can increase the risk for ventricular
rupture.
Corticosteroids are seldom used due to their substantial side effects but may be
required in patients with:
Refractory symptoms despite NSAID therapy.
Autoimmune pericarditis (especially if secondary to connective tissue disease).
Uremic pericarditis.
Prednisone dosing is highly variable but typically dosed as 1 mg/kg for 4 weeks
followed by a slow taper.
Pericardiocentesis (diagnostic and/or therapeutic) may be considered in
patients
with moderate or large pericardial effusion in patients with:
Symptoms attributable to the effusion.
Cardiac tamponade
Concern for a purulent, tuberculous, or malignant effusion
 Pericardiectomy or “pericardial window” is warranted in patients
with:

• Recurrent effusions.
• Loculated effusion, especially posterior effusions which cannot be
approached percutaneously.
• In certain patients undergoing biopsy
In patients with recurrences that are multiple, frequent, disabling,
continue for more than 2 years, and are not prevented by colchicine
and other NSAIDs and are not controlled by glucocorticoids pericardial
stripping may be necessary to terminate the illness, and
usually does so.
Paradoxical
pulse also occurs in approximately one-third of patients with constrictive
pericarditis , and in some cases of hypovolemic shock,
acute and chronic obstructive airway disease, and pulmonary embolus.
Right ventricular infarction may resemble cardiac tamponade
with hypotension, elevated jugular venous pressure, an absent
y descent in the jugular venous pulse, and, occasionally, a paradoxical
pulse
 Classification
Cardiac tamponade can be classified as:

• Acute: Typically occurs in the setting an acute cause of a small amount of

pericardial fluid in a stiff pericardium resulting in profound hemodynamic
compromise.
• Subacute: Occurs in patients with chronic effusions that slowly accumulate and
tamponade will occur once the intrapericardial pressure overcomes the
intracardiac pressure in the right atrium.
• Low pressure: Can occur in the setting of severe hypovolemia where smaller
intrapericardial pressures can overcome the decreased intracardiac pressure
leading to a decrease in cardiac output. Low-pressure tamponade refers to mild tamponade in which the
intrapericardial pressure is increased from its slightly subatmospheric
levels to +5 to +10 mmHg; in some instances, hypovolemia coexists
. As
a consequence, the central venous pressure is normal or only slightly
elevated, whereas arterial pressure is unaffected and there is no paradoxical
pulse. These patients are asymptomatic or complain of mild
weakness and dyspnea. The diagnosis is aided by echocardiography,
and both hemodynamic and clinical manifestations improve after
pericardiocentesis.
• Simultaneous RV and LV pressure tracings in constrictive pericarditis.
Note the prominent dip and plateau (square root sign), particularly post-
PVC.
A common diagnostic dilemma is the distinction between pericardial
constriction and restrictive cardiomyopathy.
Decreased compliance of either the pericardium or myocardium leads to similar
defects in ventricular filling, and substantial overlap exists in signs, symptoms,
and hemodynamic measurements.
The distinction is critical, however, as patients with restrictive cardiomyopathy
carry an exceptionally high mortality risk with cardiac surgery.
Restrictive cardiomyopathy and constriction can be present in the same patient
(e.g., after chest radiation).
The most sensitive (97%) and specific (100%) catheterization criterion for
constrictive pericarditis is a systolic area index >1.1 (the ratio of RV to LV
systolic pressure-time area in inspiration versus expiration)
Surgical pericardiectomy (stripping) is the definitive therapy of choice.
• The operative mortality rate can be as high as 20%.
• The majority of patients report symptomatic improvement with pericardiectomy
Surgery should be performed early, as constrictive pericarditis is a progressive
disease, and patients with poor functional class are at higher risk of perioperative
death.
No specific findings of constrictive pericarditis are present on the
ECG. Nonspecific T wave abnormalities, reduced voltage, and left
atrial abnormality may be seen. Atrial fibrillation is very common.
On chest radiography the cardiac silhouette can be enlarged
because of a coexisting pericardial effusion. Pericardial calcification
is seen in a minority of patients and suggests tuberculosis (Fig. 71-11)
but is not by itself diagnostic of constrictive physiology. Pleural
effusions are common and can be an initial sign. If left-sided heart
filling pressures are markedly elevated, pulmonary
vascular congestion and redistribution can
be present.
M-mode and two-dimensional transthoracic
and Doppler echocardiographic techniques
remain the key imaging modalities for the evaluation
of constrictive pericarditis (see Chapter 14).
Major findings include pericardial thickening,
abrupt displacement of the interventricular septum
during early diastole (septal “bounce”),35,36,62 and
signs of systemic venous congestion such as dilation
of the hepatic veins and distention of the inferior VC
The right atrial pressure
tracing shows a preserved x descent, a prominent y descent, and
roughly equal a and v wave heights, with a resultant M or W configuration.
RV and LV pressures reveal an early, marked diastolic dip
followed by a plateau (“dip and plateau” or “square root” sign)
(Fig. 71-12). As a manifestation of the exaggerated ventricular interdependence,
there is increased respiratory variation in LV and RV
systolic and diastolic pressure. This has been quantified by using the
“systolic area index,” the ratio of RV to LV systolic pressure times
area64 in inspiration versus expiration. A ratio greater than 1.1 strongly
suggests constriction. Pulmonary artery and RV systolic pressures are
often modestly elevated, in the 35– to 45–mm Hg range. Greater
elevation of pulmonary artery pressure is not a feature of constriction
and casts doubt on the diagnosis
. Hypovolemia, such as that caused
by diuretic therapy, can mask the hemodynamic findings. Rapid infusion
of 1 liter of normal saline over a period of 6 to 8 minutes may
reveal typical features. SV is almost always reduced, but resting
cardiac output can be preserved because of tachycardia. Enhanced respiratory
variation in mitral inflow velocity (>25%) is seen in constriction but
varies by less than 10% in restriction
Viral pericarditis is the most common pericardial infection.1,3,4,6
Numerous viruses have been implicated (HIV is discussed separately
later). Echovirus and coxsackievirus are most common. Cytomegalovirus
has a predilection for immunocompromised patients. Other
than microscopic identification of viral particles, the most definitive
way to diagnose viral pericarditis is detection of viral DNA by PCR or
in situ hybridization in pericardial fluid or tissue
Bacterial pericarditis is usually characterized by a purulent effusion.
A wide variety of organisms are causative.1,3,4,5,72 Direct extension
from pneumonia or empyema, hematogenous spread during bacteremia,
and contiguous spread after thoracic surgery or trauma account
for most cases. The most common agents are staphylococci, pneumococci,
and streptococci. After thoracic surgery, methicillinresistant
staphylococcal pericarditis is increasing, as is the frequency
of anaerobic
organisms.72 Bacterial pericarditis can also result from
rupture of perivalvular abscesses into the pericardial space (see
. Rarely, pericardial invasion spreads along facial planes
from the oral cavity. The pericardium can become infected in the
course of meningococcal sepsis with or without concurrent meningitis.
In contrast to the usual purulent fluid, Neisseria can evoke a
sterile effusion accompanied by systemic reactions such as arthritis,
pleuritis, and ophthalmitis.
Suspected or proven bacterial pericarditis is a medical emergency,
and prompt closed pericardiocentesis or surgical drainage should be
performed.1,3,4,6,72 We recommend at least 3 to 4 days of subsequent
catheter drainage. Fluid should be stained and cultured for aerobic
and anaerobic bacteria. Staining and cultures for fungi and M. tuberculosis
should also be performed. Broad-spectrum antibiotics should
be started promptly and modified according to culture results.
Purulent pericardial effusions are likely to recur.
Thus surgical
drainage with construction of a window is often needed. In patients
with thick, purulent effusions and dense adhesions, extensive pericardiectomy
may be required to achieve adequate drainage and
prevent the development of constriction. Intrapericardial fibrinolysis
has been used in selected patients with purulent effusions and may
obviate the need for a window and minimize the later development
of constriction.
Fungal infections can rarely cause
pericarditis. These are mainly locally endemic organisms such as Histoplasma
or Coccidioides or opportunistic fungi such as Candida and
Aspergillus.1,3,6 Histoplasmosis is the most common. It is endemic in
Ohio, the Mississippi River Valley, and the western Appalachians; is
acquired by inhalation; and can infect otherwise healthy patients living
in endemic areas. Coccidiomycosis is endemic in the southwestern
part of the United States and is acquired by inhalation. Immunocompromised
patients, those taking corticosteroids or broad-spectrum
antibiotics, and drug addicts are at increased risk.
Antifungal
agents are indicated only for disseminated histoplasmosis.
Coccidiomycosis-related pericarditis occurs as a complication of progressive,
disseminated infection3,81 in chronically ill, debilitated
patients. Pericardial involvement does not occur in the self-limited
influenza-like form of the infection. Physical findings suggestive
of cardiac compression may be the first clues to the diagnosis. Treatment
of disseminated infection is with intravenous amphotericin B.
Pericardiocentesis is of course indicated for tamponade. Pericarditis
secondary to opportunistic fungi such as Candida and Aspergillus
usually occurs in patients who are immunosuppressed, receiving
broad-spectrum antibiotics, or recovering from open heart surgery,
typically in the setting of disseminated infection. The prognosis
Early post-MI pericarditis occurs 1 to 3 days and no more than a week
after the index event.1,3,6 It is due to transmural necrosis with inflammation
affecting the adjacent visceral and parietal pericardium. Pericardial
involvement is correlated with infarct size. At autopsy,
approximately 40% of patients with large Q wave MIs have pericarditis.
Early revascularization has markedly reduced the incidence of
this form of pericarditis. In a recent report,82 only 4% of patients
undergoing primary percutaneous intervention had clinical evidence
of early pericarditis.
Late pericarditis is characterized by polyserositis with pericardial
and/or pleural effusions.1,3 The syndrome was first described by
Dressler and had an estimated incidence of 3% to 4%. Its incidence has
also markedly diminished during the reperfusion era and was just 0.1%
in the same report.82 Dressler syndrome is believed to have an autoimmune
cause secondary to sensitization to myocardial cells at the time
of MI. Antimyocardial antibodies have been demonstrated.
Pericardial inflammation is localized
to the infarcted area; hence changes on the ECG usually involve
subtle re-elevation of the ST segment in the originally involved leads. An
atypical T wave evolution consisting of persistent upright T waves or
early normalization of inverted T waves may occur and appears to be
highly sensitive for early post-MI pericarditis.
 constrictive pericarditis
Kussmaul’s sign is common in chronic pericarditis but
may also occur in tricuspid stenosis, right ventricular infarction, and
restrictive cardiomyopathyThe pulse pressure is normal or reduced. A paradoxical pulse
can be detected in about one-third of cases. Congestive hepatomegaly
is pronounced and may impair hepatic function and cause jaundice;
ascites is common and is usually more prominent than dependent
edema..
The apical pulse is reduced and may retract in systole
(Broadbent’s sign). The heart sounds may be distant; an early third
heart sound (i.e., a pericardial knock, occurring at the cardiac apex
0.09–0.12 s after aortic valve closure) with the abrupt cessation of
ventricular
filling is often conspicuous
If the biopsy specimen shows a thickened pericardium after 2–4
weeks of antituberculin therapy, pericardiectomy should be carried
out to prevent the development of constriction. Tubercular cardiac
constriction should be treated surgically while the patient is receiving
antituberculous chemotherapy.