Download Acute pericarditis is the most common disease state affecting the

Acute Pericarditis
Is the most common disease state affecting the pericardium. Most cases of acute pericarditis are
idiopathic or have a viral aetiology. Other potential aetiologies include bacterial and fungal
infections, rheumatologic conditions, inflammatory bowel disease, drug reactions, malignancies,
uraemia, pregnancy and immunologic disorders. Patients typically complain of sharp central
chest pain that worsens with recumbency during swallowing and with body motion.
and is relieved by leaning forward. The pain associated with acute pericarditis may be pleuritic in
nature and may radiate to the ridge of the trapezius, a sign very specific for pericardial
inflammation.
Physical examination may reveal the pathognomonic finding for pericarditis: the pericardial
friction rub. Classically, this rub occurs in three phases. They are composed of (1) an atrial
systolic rub that precedes S1, (2) a ventricular systolic rub between S1 and S2 and coincident
with the peak carotid pulse, and (3) an early diastolic rub after S2 (usually the faintest).
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
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 Beck triad (ie, hypotension; elevated systemic venous pressure, often with jugular
venous distention; and muffled heart sounds) may be observed in patients with cardiac
tamponade, especially from sudden intrapericardial hemorrhage.
 Pulsus paradoxus is defined as 10 mm Hg decrease in arterial systolic pressure with
inspiration. It is important in patients with more slowly developing tamponade because
they may lack findings of the Beck triad.
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 best demonstrated in leads II and V3; low voltage;
absence of reciprocal ST-segment changes. ST/T ratio is greater than 0.25.
Stage II: ST segments return to baseline; T-wave flattening
Stage III: T-wave inversion
Stage IV: Gradual resolution of T-wave inversion
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. It is this
inflammation that creates the characteristic friction rub heard on auscultation, which has been
described as being "like the squeak of leather on a new saddle under a rider"
Pericardium Anatomy
The pericardium consists of an outer fibrous layer called the parietal pericardium and an inner
serosal membrane overlying the epicardial surface called the visceral pericardium. Between these
layers is a potential space normally containing approximately 20 mL of fluid, an ultrafiltrate of
plasma. Drainage occurs via the thoracic duct and the right lymphatic duct into the right pleural
space. Important functions of the pericardium include limiting acute distention of the heart,
especially in states of volume 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.
It also creates a closed chamber with subatmospheric pressure that aids atrial filling and lowers
transmural cardiac pressures.
TABLE 1
Aetiologies of Acute Pericarditis * more common
Infectious
Viral. 1-10% of cases. See idiopathic
Coxsackievirus*
Echovirus
Epstein-Barr virus
Influenza virus
Human immunodeficiency virus
Mumps virus
Bacterial. 1-8% of cases and causes purulent pericarditis
Staphylococcus
Hemophilus
Pneumococcus. Common in pre-antibiotic era.
Salmonella
Meningococcus
Syphilis
Tuberculosis 4% of cases. Approximately half the
patients develop constrictive pericarditis
Miscellaneous
Histoplasmosis
Blastomycosis
Coccidioidomycosis
Aspergillosis
Echinococcosis
Amebiasis
Rickettsia
Rheumatologic
Sarcoidosis
Lupus*
Rheumatoid arthritis
Dermatomyositis
Scleroderma
Polyarteritis nodosa
Vasculitis
Ankylosing spondylitis
Neoplastic
Metastatic
Breast
Lung
Lymphoma
Melanoma
Leukemia
Primary
Sarcomas
Mesothelioma
Drugs
Hydralazine* (Apresoline)
Procainamide* (Pronestyl)
Others
Immunologic
Celiac sprue
Inflammatory bowel disease
Other
Chest trauma
Uremia*
Myxedema
Aortic dissection
Radiation therapy
Myocardial infarction*
Postmyocardial infarction syndrome (i.e., Dressler's
syndrome, postpericardiotomy*)
Idiopathic* 26% and 86% of cases are idiopathic in
nature. No clinical features distinguish these from viral
pericarditis. Most likely, the majority of idiopathic cases
are undiagnosed viral infections.
Differential Diagnosis of Acute Pericarditis by ECG Myocardial infarction, Early repolarization,
Myocarditis
Pulmonary embolus, Cerebrovascular accident, Pneumothorax
Hyperkalemia, Pneumopericardium, Subepicardial hemorrhage, Ventricular aneurysm
Prognosis
Most cases of acute idiopathic or viral pericarditis do not recur; however, acute pericarditis may
recur if it is associated with an ongoing underlying illness such as an autoimmune disease or
uraemia. 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. On occasion,
idiopathic acute pericarditis may recur several times but will rarely lead to effusion and cardiac
tamponade or constrictive pericarditis necessitating pericardectomy. Typically, 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 during stage III of acute pericarditis.
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