Epidemiology

Although the greatest concern in patients with chest pain is usually vascular causes of chest pain—acute coronary syndrome, pulmonary embolism, and aortic dissection—other less common, but potentially deadly illnesses must be considered, including pericarditis, pericardial tamponade, and myocarditis.

Acute pericarditis is often subclinical, so its incidence is uncertain. However, rough estimates range from 2% to 6%,¹ and this disorder may be responsible for as many as 1 in every 1000 hospital admissions.² Although acute pericarditis is not usually deadly, it can be painfully disabling if not treated appropriately.

Pericardial tamponade is a potentially deadly result of pericardial effusion. Such an effusion can develop from pericardial inflammation or cardiac trauma. Unfortunately, the early features of tamponade can mimic those of other diseases and lead to initial misdiagnosis.

Acute myocarditis is relatively uncommon, but it is a devastating condition that can occur and progress quickly, with little warning. The initial findings can vary from mild, viral-type symptoms to fulminant cardiogenic shock.

Pathophysiology

The pericardium is the layer of tissue surrounding the heart. It consists of two layers, a serous inner layer (visceral pericardium) and a fibrocollagenous outer layer (parietal pericardium). The pericardium completely encloses the ventricles and the right atrium; a portion of the left atrium remains outside the sac. A thin layer of plasma fluid (usually 15 to 30 mL) separates the visceral and parietal pericardial layers and acts as a lubricant. The main function of the pericardium appears to be provision of ligamentous stability to withstand forces against the heart. It also provides some shielding for the heart. Despite these apparent functions, however, the majority of patients who undergo pericardiectomy do not appear to suffer any decrease in cardiac performance or other ill effects.

Pericarditis refers to inflammation of the layers of the pericardium. It has many possible causes (Box 60.1), but in most cases the cause is unknown. In the majority of these idiopathic cases the presumed cause is viral, although most attempts to prove a viral cause have low yield. The most common viral cause is coxsackievirus B. The most common cause of pericarditis worldwide is tuberculosis.³

Presenting Signs and Symptoms

Differential Diagnosis and Medical Decision Making

A thorough differential diagnosis of a patient with chest pain is described in Chapter 54. However, the most important initial consideration should always be the deadly causes of chest pain: pericarditis, acute coronary ischemia or infarction, thoracic aortic dissection, and pulmonary embolism. Table 60.1 lists some historical and physical examination features that are helpful in distinguishing among these conditions. Distinction among these causes of chest pain is critical in terms of treatment; patients with pulmonary embolism or myocardial infarction often require treatment with anticoagulants and thrombolytics, medications that can be deadly in patients with acute pericarditis or aortic dissection.

The diagnosis of acute pericarditis is based primarily on the clinical findings. In many cases an electrocardiogram (ECG) is helpful in confirming the diagnosis. Sound knowledge of the ECG findings in patients with acute pericarditis is critical, as well as some findings that help in diagnosing pericarditis versus myocardial infarction (see Table 60.1). Classically, pericarditis evolves through four ECG stages as described in Table 60.2. The first stage of acute pericarditis, characterized by diffuse ST-segment elevation and PR-segment depression or downsloping (Fig. 60.1), is the most common stage encountered in the emergency department (ED). The ST segments should be concave upward; a convex upward (“tombstone”) morphology virtually excludes the diagnosis of pericarditis and rules in acute myocardial infarction. ST-segment depression may be present in leads aVR and V₁ in a patient with pericarditis but is unlikely to be present in any of the other 10 leads. In fact, the presence of ST-segment depression in any of the other 10 leads should be considered the “reciprocal” changes of acute myocardial infarction.

Table 60.2 Electrocardiographic Stages of Acute Pericarditis

Fig. 60.1 Acute pericarditis.

The electrocardiogram demonstrates diffuse ST-segment elevation with PR-segment depression in multiple leads.

These four stages generally progress over the course of days to weeks. The ECG changes in the second and third stages usually occur in the same leads in which abnormalities in the initial stage occurred.

Although the abnormalities noted on an ECG are typically described as “classic” for acute pericarditis, physicians should be aware that these findings are typical only for acute viral pericarditis. Other forms of pericarditis less commonly cause PR-segment depression and occasionally cause less pronounced ST-segment elevation. In these cases, the diagnosis must be based purely on the clinical rather than the ECG findings.

Laboratory studies are rarely helpful in the diagnosis of acute pericarditis. Patients may have an elevated white blood cell count because of pain or infection (or both). Other serum markers of inflammation, including the erythrocyte sedimentation rate and C-reactive protein value, are often elevated, but such elevations are nonspecific. Cardiac biomarkers may be minimally elevated but should not demonstrate the rise and fall typical of myocardial infarction. Chest radiography is also rarely helpful in the diagnosis of acute pericarditis; it is used mainly to evaluate for alternative causes of chest pain (e.g., pneumonia, aortic dissection).

Echocardiography can be useful in distinguishing between acute pericarditis and acute myocardial infarction. Echocardiograms in patients with pericarditis lack the focal wall motion abnormalities that are typical of echocardiograms in those with myocardial infarction. Echocardiography is also useful to look for evidence of pericardial effusion, a potential complication of acute pericarditis (see later). If a large pericardial effusion is present, pericardiocentesis (ultrasonographically guided in a stable patient) can be performed to obtain fluid for testing for infections and cytologic analysis.

Treatment

Treatment of patients with acute pericarditis should be targeted at the underlying cause. The majority of patients with viral, rheumatologic, posttraumatic, or idiopathic pericarditis are effectively treated with high-dose aspirin (2 to 4 g daily) or nonsteroidal antiinflammatory drugs (NSAIDs). Ibuprofen is effective in most cases and has fewer side effects than other NSAIDs; the pain usually improves significantly within days with ibuprofen therapy. If the patient’s symptoms persist, an alternative NSAID is indicated. Indomethacin is often used for severe cases because of its stronger antiinflammatory effect, although it should be avoided in patients with a history of ischemic heart disease because it may decrease coronary blood flow.^4,7 Evidence now suggests that addition of colchicine (1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/day for 3 months) to the standard regimen is effective in hastening the resolution of acute symptoms and also preventing recurrence rates, regardless of the cause of the pericarditis.⁸ Colchicine is also effective in cases of recurrent pericarditis.^9,10 The use of corticosteroids is generally reserved for recurrent cases of pericarditis that are unresponsive to aspirin or NSAIDs plus colchicine. Initiation of steroids early in the course of first-time pericarditis may actually be an independent risk factor for recurrence.⁸

Patients with bacterial or other nonviral infectious causes of pericarditis should be treated aggressively with antimicrobial therapy. Large infected pericardial effusions require drainage as well. Management of neoplastic causes of pericarditis should be targeted at treating the underlying malignancy. Patients with uremic pericarditis require urgent hemodialysis.

Follow-Up and Next Steps in Care