constriction.3
More than half of patients with pericarditis will present
complaining of chest pain that may radiate to the back, neck
or shoulders.4 If pain radiates to one or both trapezius muscle
ridges, it may be due to pericarditis because the phrenic nerve
(which innervates these muscles) traverses the pericardium.3
In contrast to acute coronary syndromes, pericardial pain typically
worsens with inspiration and is improved while sitting up
and leaning forward. Approximately 25–40% of patients with
pericarditis will complain of dyspnea, and 17% of fever.4
The most common physical finding in patients with pericarditis
is a pericardial friction rub, which occurs in approximately
50–85% of cases.3–5 A pericardial friction rub is best
heard at the lower sternal border or apex when the patient is
sitting forward on his or her hands and knees. Other findings
on physical exam may include fever (may reach 104◦F/40◦C),
cardiac dysrhythmias (e.g., premature atrial and ventricular
contractions), tachypnea and dyspnea.5 Individuals with associated
cardiac tamponade may show jugular venous distension,
tachycardia, hypotension or pulsus paradoxus.
The 12-lead ECG in patients with acute pericarditis classically
shows widespread upward concave ST-segment elevation
and PR-segment depression.3 In addition, lead aVR
on the ECG can demonstrate ST-segment depression and
PR-segment elevation.1 The ECG abnormalities evolve
through four classic stages.6 Stage I is characterized by
ST-segment elevation, prominent T waves and PR-segment
depression. Stage II is characterized by a normalization of
the initial abnormalities, namely resolution of the ST-segment
elevation. Stage III involves T wave inversion, usually in the
same distribution where ST-segment elevation was encountered.
Finally, Stage IV is a normalization of all changes with
a return to the baseline ECG. Persistent ST-segment elevation
and pathologic Q waves are not encountered in patients
with pericarditis – these ECG findings should suggest another
etiology.6