Intro 

The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a (potential)
space, the pericardial cavity. In healthy individuals, the pericardial cavity contains 15 to 50 mL of an
ultrafiltrate of plasma.

Diseases of the pericardium present clinically in one of four ways:

1.Acute fibrinous pericarditis

2.Pericardial effusion without major hemodynamic compromise

3.Cardiac tamponade

4.Constrictive pericarditis

Acute pericarditis is recorded in about 0.1 percent of hospitalized patients and 5 percent of patients admitted
to the Emergency Department for non-acute myocardial infarction chest pain

Etiology

The pericardium may be involved in a large number of systemic disorders or may be diseased as an isolated
process (table 1).

In a series from a tertiary referral center of 260 patients, the following diagnoses were obtained:

• Viral (adenovirus, enteroviruses, CMV, influenza, HepB virus, and HSV )— 21 %

• Tuberculous — 4 %
• Other bacterial — 6 %
• "Autoreactive" (immune-mediated) — 23 %
• Uremia — 6 %
• Neoplastic — 35 %
• Idiopathic — 4 %

Diagnosis

Table
Chest pain:

• typically fairly sudden in onset and occurs over the anterior chest
• often pleuritic in nature, being sharp and exacerbated by inspiration.
• However, dull, oppressive pain, which is difficult to distinguish from that of myocardial ischemia,
can occur.
• The pain may decrease in intensity when the patient sits up and leans forward and may radiate.

Pericardial friction rub:

• Highly specific for acute pericarditis. The sensitivity is variable

• Generated by friction of the two inflamed layers of the pericardium
• Pericardial friction rubs occur during the maximal movement of the heart within its pericardial sac.
Thus, the classic friction rub consists of three phases, corresponding to movement of the heart
during atrial systole, ventricular systole, and in the rapid filling phase of early ventricular diastole.
• Pericardial rubs have a superficial scratchy or squeaking sound that is best heard with the
diaphragm of the stethoscope best heard over the left sternal border with patient leaning
Cardiac biomarkers:

• Acute pericarditis is often associated with increases in serum biomarkers for myocardial injury such
as troponin I (cTnI) with or without increased MB fraction of creatine kinase (CK-MB). Such patients
should be considered to have myopericarditis.

Signs of inflammation:
• Laboratory signs of inflammation are common in patients with acute pericarditis. These include
elevations in the white blood cell count, ESR and CRP--supports the diagnosis, although data on
the sensitivity of this finding is lacking.

Echocardiogram:

• often normal in patients with the clinical syndrome of acute pericarditis unless it is associated with a
pericardial effusion. While the finding of a pericardial effusion in a patient with known or suspected
pericarditis supports the diagnosis, the absence of a pericardial effusion or other echocardiographic
abnormalities does not exclude it.
Chest x-ray:
• typically normal in patients with acute pericarditis. Although patients with a substantial pericardial
effusion may exhibit an enlarged cardiac silhouette with clear lung fields

The presence of pericarditis should also be suspected in the presence of persistent fever in patients with
pericardial effusion or unexplained, new radiographic cardiomegaly.

Because the same viruses that are responsible for acute pericarditis can also cause myocarditis, it is not
uncommon to find some degree of myocardial involvement in patients with acute pericarditis. The terms
"myopericarditis" and "perimyocarditis" are sometimes used interchangeably or they can be used to indicate
the dominant site of involvement.

ECG evolution:

The electrocardiogram in acute pericarditis evolves through four stages:

• Stage 1, seen in the first hours to days, is characterized by diffuse ST elevation (typically concave
up) with reciprocal ST depression in leads aVR and V1.
• Stage 2 is characterized by normalization of the ST and PR segments.
• Stage 3 is characterized by the development of diffuse T wave inversions, generally after the ST
segments have become isoelectric.
• Stage 4, the ECG may become normal or the T wave inversions may persist indefinitely ("chronic"
pericarditis).

Vs. MI:
• The ST segment elevation in acute pericarditis rarely exceeds 5 mm
• The distribution of ST elevation is different. ST segment elevations in STEMI are characteristically
limited to either the anterolateral leads (I, aVL, V1 to V6) or the inferior (II, III, aVF) leads because
of the localized area of the infarct. The pericardium envelops the heart, and the ST-T changes are
therefore more generalized, being present in most of the chest leads as well as leads I, aVL, II, III,
and aVF.
• Acute STEMI is often associated with reciprocal ST segment changes, which are not seen with
pericarditis except in aVR and V1.
• ST segment elevation and T wave inversions do not generally occur simultaneously in pericarditis,
although they commonly do so in acute STEMI.
• Pathologic Q waves, which often occur in STEMI, are generally not seen in pericarditis. The
abnormal Q waves in MI reflect the loss of positive depolarization voltages because of myocardial
necrosis. Pericarditis, on the other hand, generally causes only superficial inflammation, not frank
myocardial necrosis.
Initial Mgmt:

Because of the relatively benign course associated with the common causes of pericarditis, it is not
necessary to perform a full diagnostic evaluation in all patients with acute pericarditis.

Initial efforts should focus upon excluding:

• a significant effusion or tamponade (with echocardiography)

• identification of patients at risk for tuberculosis or purulent pericarditis)
• r/o coronary disease, myocardial ischemia must be ruled out by appropriate

Initial history and physical examination:

• This evaluation should consider disorders that are known to involve the pericardium, such as
uremia, recent myocardial infarction (MI), and prior cardiac surgery.
• The examination should pay particular attention to auscultation for a pericardial friction rub and the
signs associated with tamponade.

Echocardiography:
• in all cases, and should be considered on an urgent basis if tamponade is suspected
• Even a small effusion can be helpful in confirming the diagnosis of pericarditis, although the
absence of an effusion does not exclude the diagnosis.
An ECG in all cases
Chest x-ray in all cases
PPD
Antinuclear antibody titer in selected cases
HIV serology in selected cases
Blood cultures if fever higher than 38ºC (100.4ºF) or signs of sepsis

Determination of risk and need for hospitalization:

• Many physicians admit all new cases of acute pericarditis to the hospital, but this may not be
necessary.
• A patient with simple uncomplicated acute pericarditis can undergo initial evaluation in a same day
hospital facility or clinic, although outpatient follow-up is required.
• On the other hand, patients with high risk features are at increased risk of short-term complications
and have a higher likelihood of a specific disease--Hospital admission is indicated for
administration of appropriate therapy and thorough evaluation of etiology (eg, pericardiocentesis for
tamponade or to identify a purulent effusion).

Features of high risk include

Fever (>38ºC [100.4ºF]) and leukocytosis

Evidence suggesting cardiac tamponade
A large pericardial effusion (ie, an echo-free space of more than 20 mm)
Immunosuppressed state
A history of oral anticoagulant therapy
Acute trauma
Failure to respond within seven days to NSAID therapy
Elevated cardiac troponin, suggestive of myopericarditis
Treatment

Identifiable cause (eg, bacterial infection or malignancy), management is focused upon the underlying
disorder and, if necessary, drainage of an associated pericardial effusion.

Idiopathic or viral pericarditis — In patients with acute pericarditis that is idiopathic or due to a presumed
viral infection, we suggest the following approach:

• NSAIDs for all patients without a contraindication. Because these drugs do not alter the natural
history of pericarditis, treatment duration is based upon the persistence of symptoms, which is
usually for one week or less. Intravenous administration of NSAID may be particularly useful to
control acute and severe symptoms at the beginning of therapy.

o Ibuprofen — Depending upon the severity of the pericarditis and individual medication
response, 300 to 800 mg of ibuprofen every six to eight hours, which can be continued for
days or weeks for recurrent or incessant attacks as needed.
o Aspirin — An alternative protocol consists of aspirin (800 mg every six to eight hours
followed by gradual tapering of 800 mg every week for a treatment period of three to four
weeks

o Patients treated with aspirin or another NSAID should also receive gastrointestinal
protection (eg, a proton pump inhibitor

We suggest that colchicine not be used routinely in the management of a first episode of acute
pericarditis. The majority of patients have prompt resolution of symptoms without recurrent
pericarditis when treated with NSAIDS alone. However, based upon a reduced rate of recurrent
pericarditis and a low incidence of side effects, some physicians and patients may choose to add
colchicine (1 to 2 mg on the first day, followed by 0.5 once or twice daily for three months) as an
adjunct to NSAID therapy.

Post-MI pericarditis:

• ASA (no other NSAID or glucocorticoid)

• Because of the possible influence of antiinflammatory agents on the healing process after an MI,
patients with pericarditis after an acute MI are approached differently.
• Although the evidence of potential harm from glucocorticoids and NSAIDs other than aspirin is
modest, there is no evidence that these medications improve outcomes

Acute pericarditis due to connective tissue disease

Autoreactive (immune-mediated) pericarditis
Idiopathic/Viral Pericarditis refractory to NSAIDS/Colchicine
Uremic pericarditis:

• Glucocorticoids