Electrocardiographic Manifestations and

Differential Diagnosis of Acute Pericarditis

MARK A. MARINELLA, M.D., Wright State University School of Medicine, Dayton, Ohio

Acute pericarditis has many potential etiologies and typically presents as sharp central
chest pain that worsens with recumbency and is relieved by leaning forward. The
pathognomonic physical finding of acute pericarditis is the pericardial friction rub,
which is usually auscultated along the lower left sternal border. The electrocardiogram
(ECG) is a useful, simple tool that may aid in the diagnosis of acute pericarditis. Typi-
cal ECG findings include diffuse concave-upward ST-segment elevation and, occasion-
ally, PR-segment depression. ECG changes of both acute myocardial infarction and early
repolarization can appear similar to ECG changes of acute pericarditis. However, these
conditions can usually be excluded by an accurate history, physical examination and
recognition of a few key features on the ECG.

A
cute pericarditis is the most
common disease state affecting
the pericardium. Most cases of
acute pericarditis are idiopathic
or have a viral etiology.1,2 Other
potential etiologies include bacterial and fungal
infections, rheumatologic conditions, in-
flammatory bowel disease, drug reactions,
malignancies, uremia, pregnancy and immuno-
logic disorders (Table 1).1,3-5 Patients typically
complain of sharp central chest pain that wors-
ens with recumbency and is relieved by leaning
forward. The pain associated with acute peri-
carditis may be pleuritic in nature and may radi-
ate to the ridge of the trapezius, a sign very spe-
cific for pericardial inflammation.6
Physical examination may reveal the pathog-
nomonic finding for pericarditis: the pericar-
dial friction rub. Classically, this rub occurs in
three phases corresponding with atrial systole,
ventricular systole and ventricular diastole.
However, it is uncommon for all three phases
to be heard clinically and, at times, the rub
may be evanescent.2 The friction rub is best
appreciated by firmly applying the diaphragm
to the left lower sternal border with the
patient leaning forward after an exhalation.
The electrocardiogram (ECG) is very useful
This article in the diagnosis of acute pericarditis. Character-
exemplifies the AAFP istic manifestations of acute pericarditis on
1997-98 Annual Clinical
Focus on prevention
ECG most commonly include diffuse ST-seg-
and management of ment elevation. However, other conditions may
cardiovascular disease. have ECG features similar to those of acute peri-
carditis. These conditions most commonly
include acute myocardial infarction and early
repolarization. Since these and other conditions
require distinctly different treatments, physi-
cians should be able to recognize the typical
manifestations of acute pericarditis. This article
reviews some of the common ECG findings
associated with acute pericarditis as well as cri-
teria to differentiate acute pericarditis from
other conditions.
Illustrative Case
A previously healthy 52-year-old man pre-
sented to the emergency department with a his-
tory of sharp, pleuritic central chest pain occur-
ring over the past several hours. The pain began
at rest, was exacerbated in the supine position
and was relieved by leaning forward. There was
no history of radiation of the pain, dyspnea,
diaphoresis, palpitations, vomiting, or chills or
fever. He had no prior history of pain or any
chest trauma. A few weeks previously, he had
noted a sore throat without other symptoms.
He had no previous medical problems and took
no medications. He did not smoke, consume
alcohol or use illicit drugs. He had no known
risk factors for human immunodeficiency virus
infection. There was no family history of heart
disease or collagen vascular disease.
The patient’s pulse rate was 80 per minute,
his respiration rate was 14 per minute, his
blood pressure was 132/80 mm Hg, and his
temperature was 36.5°C (97.8°F). There was no

FEBRUARY 15, 1998 / VOLUME 57, NUMBER 4 AMERICAN FAMILY PHYSICIAN 699
 TABLE 1
Etiologies of Acute Pericarditis
Acute Pericarditis
Infectious Neoplastic
Viral Metastatic
Coxsackievirus* Breast
Echovirus Lung
Epstein-Barr virus Lymphoma
Influenza virus Melanoma
pulsus paradoxus or jugular venous distention. Human Leukemia
Cardiac examination revealed a regular rate immunodeficiency Primary
and rhythm without murmurs; however, a virus Sarcomas
two-phase friction rub was heard at the left Mumps virus Mesothelioma
Bacterial Drugs
lower sternal border. The remainder of the
Staphylococcus Hydralazine*
physical examination was normal.
Hemophilus (Apresoline)
The following laboratory results were nor- Pneumococcus Procainamide*
mal: blood urea nitrogen, creatinine, elec- Salmonella (Pronestyl)
trolytes, liver function tests, hemoglobin mass Tuberculosis Others
concentration, and white blood cell count. Meningococcus Immunologic
The erythrocyte sedimentation rate was 22 Syphilis Celiac sprue
mm per hour, and the antinuclear antibody Miscellaneous Inflammatory bowel
Histoplasmosis disease
test was negative. A chest radiograph and
Blastomycosis Other
echocardiogram were normal. The ECG Coccidioidomycosis Chest trauma
revealed diffuse concave-upward ST-segment Aspergillosis Uremia*
elevation with PR depression (Figure 1). A Echinococcosis Myxedema
diagnosis of acute pericarditis was estab- Amebiasis Aortic dissection
lished, with the most likely etiology being Rickettsia Radiation therapy
either idiopathic or postviral. Viral serologies Rheumatologic Myocardial infarction*
Sarcoidosis Postmyocardial
were not performed. The patient was treated
Lupus* infarction syndrome
with aspirin, 650 mg every six hours, and (i.e., Dressler’s
Rheumatoid arthritis
showed marked improvement by the follow- Dermatomyositis syndrome,
ing day. At the two-week follow-up visit, the Scleroderma postpericardiotomy*)
patient was doing well. Polyarteritis nodosa Idiopathic*
Vasculitis
Anatomy and Physiology Ankylosing spondylitis
of the Pericardium
The pericardium consists of an outer *—Some of the more common etiologies of peri-
fibrous layer called the parietal pericardium carditis.
and an inner serosal membrane overlying the Information from references 1, 3-5.

FIGURE 1. ECG of a patient with acute pericarditis. Diffuse concave-upward ST-segment elevation, ST-
segment depression in aVR, and PR-segment depression is best demonstrated in leads II and V3. Note
lack of reciprocal ST-segment changes, an important feature differentiating acute pericarditis from
acute myocardial infarction. Also note that the ST/T ratio is greater than 0.25, a finding frequently
indicative of acute pericarditis.

700 AMERICAN FAMILY PHYSICIAN VOLUME 57, NUMBER 4 / FEBRUARY 15, 1998

epicardial surface called the visceral peri-
cardium. Between these layers is a potential
space normally containing approximately
20 mL of fluid, an ultrafiltrate of plasma.3,7
The majority of the parietal pericardium is
composed of collagen fibrils arranged similar
to an accordian, enhancing the elastic proper-
ties of the structure. On the ultrastructural
level, the pericardium contains numerous
villi and cilia that enhance fluid resorption
and facilitate movement of pericardial sur-
faces over one another. Important functions
of the pericardium include limiting acute dis-
tention of the heart, especially in states of vol-
ume overload, maintaining the heart in an
optimal shape and position, and acting as a
buttress against inflammation to prevent it
from spreading to adjacent structures.3,8
Classic acute or “dry” pericarditis usually
results in deposition of a fibrinous material
with a characteristic “bread-and-butter”
appearance likened to pulling two pieces of
buttered bread apart. The vascularity of the
pericardium is increased, which may impart
a gross red appearance with diffuse fibrin
deposition and neutrophils present on
microscopic examination.9 It is this inflam-
mation that creates the characteristic fric-
tion rub heard on auscultation, which has
been described as being “like the squeak of
leather on a new saddle under a rider, or
TABLE 2
Stages of Acute Pericarditis on ECG
Stage Changes on ECG
Stage I Diffuse concave-upward ST-segment elevation with concordance of T waves; ST-segment
depression in aVR or V1; PR-segment depression; low voltage; absence of reciprocal
ST-segment changes
Stage II ST segments return to baseline; T-wave flattening
Stage III T-wave inversion
Stage IV Gradual resolution of T-wave inversion
ECG = electrocardiogram.
Information from references 9 and 10.
FEBRUARY 15, 1998 / VOLUME 57, NUMBER 4
The characteristic pericardial friction rub heard on ausculta-
tion comes from fibrinous material deposited between the
two inflamed layers of the pericardium.
grating in the knee joint on moving the
patella over the femoral condyles.”6
Electrocardiographic
Manifestations
The ECG is useful in the diagnosis of acute
pericarditis, with abnormalities found in
approximately 90 percent of cases. Changes
on ECG classically occur in four stages (Table
2).9,10 Not all cases of pericarditis include each
of these four stages. In fact, all four stages are
present in only 50 percent of patients or less.
Stage I typically occurs during the first few
days of pericardial inflammation and is
mainly characterized by diffuse ST-segment
elevation. This stage may last up to two weeks.
Stage II is characterized by return of the ST
segments to baseline and flattening of the T
wave and may last from days to several weeks.
Stage III usually begins at the end of the sec-
ond or third week and is characterized by
inversion of the T waves in the opposite direc-
tion of the ST segment; this stage may last sev-
eral weeks. Stage IV represents the gradual res-
olution of the T-wave changes and may last up
to three months.11
AMERICAN FAMILY PHYSICIAN 701
Acute Pericarditis
The most sensitive ECG change in acute pericarditis is diffuse
ST-segment elevation; a very specific change is depression of
the PR segment in all leads except aVR and V1.
The most sensitive ECG change character-
istic of acute pericarditis is ST-segment eleva-
tion, which reflects the abnormal repolariza-
tion that develops secondary to pericardial
inflammation. There may also be ST-segment
depression in leads aVR and V1. Typically,
there are no changes during depolarization,
so in the absence of underlying cardiac dis-
ease, the P wave and QRS complexes are nor-
mal.2 Depression of the PR segment is very
specific of acute pericarditis and is attributed
to subepicardial atrial injury and occurs in all
leads except aVR and V1. These leads may ex-
hibit PR-segment elevation.2,11,12
The pattern of ST-segment elevation is
important in the diagnosis of acute pericarditis.
The ST-segment elevation that occurs during
acute pericarditis is usually “concave,” com-
pared with the “convex” appearance of the ST
segment that occurs during the acute injury
stage of a myocardial infarction. Another
important feature of acute pericarditis is the
widespread ST-segment elevation not corre-
sponding with any specific arterial territory,
which usually occurs in association with acute
myocardial infarction.2 Also, reciprocal changes
are absent in acute pericarditis, although they
are frequently found with acute myocardial
infarction. The ST segments in acute pericardi-
tis return to baseline in a few days and are fol-
The Author
MARK A. MARINELLA, M.D., is an assistant clinical professor of internal medicine at
Wright State University School of Medicine, Dayton, Ohio. Dr. Marinella is a graduate
of Wright State University School of Medicine and completed a residency in internal
medicine at the University of Michigan Medical Center, Ann Arbor.
Address correspondence to Mark A. Marinella, M.D., 33 West Rahn Rd., Suite 201,
Dayton, OH 45429. Reprints are not available from the author.
702 AMERICAN FAMILY PHYSICIAN
lowed by diffuse T-wave inversion, in conjunc-
tion with the ST segment at baseline.11
Another feature that may aid in differenti-
ating acute pericarditis from acute myo-
cardial infarction is the absence of Q waves
and the absence of T-wave inversion at the
time of ST-segment elevation, both of which
classically occur with acute myocardial
infarction.2 Loss of R-wave progression may
occur with acute myocardial infarction, but
this feature is not present with acute peri-
carditis. Low voltage (i.e., decreased ampli-
tude of the QRS complex) may also be pre-
sent. Arrhythmias are uncommon in acute
pericarditis. In one large study,13 no ar-
rhythmias occurred in patients without un-
derlying cardiac disease.
Differential Diagnosis
of Acute Pericarditis by ECG
Acute pericarditis exhibits characteristic
changes on ECG that usually enable one to
make the diagnosis readily. There are other
conditions that the clinician needs to con-
sider in the differential diagnosis of acute
pericarditis by ECG (Table 3). However, find-
ings on the history and physical examination
and on laboratory assessment usually narrow
the diagnostic possibilities. Two conditions
that are commonly confused with acute peri-
TABLE 3
Differential Diagnosis
of Acute Pericarditis by ECG
Myocardial infarction
Early repolarization
Myocarditis
Pulmonary embolus
Cerebrovascular accident
Pneumothorax
Hyperkalemia
Pneumopericardium
Subepicardial hemorrhage
Ventricular aneurysm
ECG = electrocardiogram.
VOLUME 57, NUMBER 4 / FEBRUARY 15, 1998
FIGURE 2. Single electrocardiographic complexes comparing (left) acute pericarditis, (center)
early repolarization and (right) injury pattern of acute myocardial infarction. Note the degree of
ST-segment elevation is greater in the pericarditis complex than in the early repolarization com-
plex. Important findings of acute infarction include the presence of Q waves and a more convex
upward ST segment, both of which are present in the right complex.

carditis include acute myocardial infarction Another useful clue in differentiating

and early repolarization (Figure 2).
Early repolarization is a normal variant that
occurs commonly in young males, especially
blacks, and does not evolve with the stages of
acute pericarditis.2 Early repolarization is dis-
tinguished by ST-segment elevation limited to
the precordial leads, elevation of the ST seg-
ment in V1, an isoelectric ST segment in lead
V6, notching of the terminal aspect of the
QRS complex, and a shift to baseline of the ST
segments with exercise.10,11
acute pericarditis from early repolarization
is the ST/T ratio in lead V6. This is calcu-
lated by dividing the millimeters of ST-seg-
ment elevation by the millimeters to the
tallest point of the T wave. Each value is
measured from the isoelectric point. An
ST/T ratio of greater than 0.25 in lead V6
suggests acute pericarditis.10,14 Table 4 lists
findings on ECG that are characteristic of
acute pericarditis, acute myocardial infarc-
tion and early repolarization.

TABLE 4
Comparison of ECG Changes Associated with
Acute Pericarditis, Myocardial Infarction and Early Repolarization

ECG finding Acute pericarditis Myocardial infarction Early repolarization

ST-segment shape Concave upward Convex upward Concave upward

Q waves Absent Present Absent
Reciprocal ST-segment changes Absent Present Absent
Location of ST-segment elevation Limb and precordial Area of involved Precordial leads
leads artery
ST/T ratio in lead V6* > 0.25 N/A < 0.25
Loss of R-wave voltage Absent Present Absent
PR-segment depression Present Absent Absent

ECG = electrocardiogram; N/A = not applicable.

*—See text for further information.

FEBRUARY 15, 1998 / VOLUME 57, NUMBER 4 AMERICAN FAMILY PHYSICIAN 703
Acute Pericarditis
Symptoms subside within two weeks and ECG changes resolve
over a period of weeks to months; in the absence of ongoing
underlying disease, most cases of pericarditis do not recur.
Follow-up
Most cases of acute idiopathic or viral peri-
carditis do not recur; however, acute pericardi-
tis may recur if it is associated with an ongoing
underlying illness such as an autoimmune dis-
ease or uremia. Symptoms usually subside
within two weeks; however, up to 15 percent of
patients may experience a recurrence in the first
few months following the initial episode.1,5,15
On occasion, idiopathic acute pericarditis may
recur several times but will rarely lead to effu-
sion and cardiac tamponade or constrictive
pericarditis necessitating pericardectomy.3 Typ-
ically, physicians should schedule a follow-up
visit with these patients two weeks after the
onset of their illness unless problems arise
sooner. An ECG should be considered at four
weeks, bearing in mind that residual T-wave
inversion may be present for several weeks dur-
ing stage III of acute pericarditis.1,5,10,15
. 14. Ginzton LE, Laks MM. The differential diagnosis of
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