Listen for a grating, squeaking, or creaking sound. Because the rub may be transient, auscultation repeated over a period of several hours may be necessary to establish its presence. Although the pericardial rub is diagnostic of pericarditis, it does not rule out an associated MI. Laboratory and ECG findings usually help pinpoint a diagnosis of MI.

As part of the history and physical examination, consider the characteristics of the pain. The pain of pericarditis is typically sharp or stabbing and most often substernal. Although frequently of sudden onset, it may also gradually increase in intensity. The pain is often pleuritic, and it usually worsens when the patient breathes deeply, coughs, or lies down. It tends to lessen when the patient sits up or leans forward. These characteristics help differentiate pericarditis pain from that associated with myocardial ischemia. In a significant proportion of cases, however, the pain of pericarditis is indistinguishable from that of myocardial ischemia or infarction.

The pain caused by pericarditis may radiate (rarely be confined) to the ridge of the trapezius muscle—a classic and very specific sign. It can also mimic angina, radiating to the jaw or shoulders. Therefore, distinguishing between shoulder pain and discomfort originating in the trapezius muscle is important. Pain due to pericarditis can persist for hours or even days, whereas angina will usually improve spontaneously or with reduced exertion.

Fever can serve as a diagnostic clue, depending on when it began. In patients with viral or idiopathic pericarditis, the fever usually precedes the pain. In those with MI, the pain more often precedes the fever, which in this case is part of the response to myocardial necrosis.

TESTS FOR DIAGNOSTIC CONFIRMATION

Appropriate laboratory tests in a patient with possible pericardial symptoms include a CBC and differential. A bacterial or other infectious etiology may cause an elevated WBC count. The ESR and C-reactive protein level are invariably elevated in patients with pericarditis. Other laboratory studies should include determination of serum urea nitrogen, serum creatinine, electrolyte, creatine kinase isoenzyme MB (CK-MB), and cardiac enzyme levels and liver function tests. Troponin I is frequently elevated but remains below the threshold for MI unless the patient has myopericarditis. These small elevations of CK-MB and troponin I have no prognostic significance. Depending on the suspected etiology, tests for antinuclear antibodies and other indicators of autoimmune disease might be appropriate. If tuberculosis is a serious possibility, a skin test, sputum culture, and even pericardial biopsy should be considered.

A chest radiograph can help rule out a tumor in the area of the heart or a new pericardial effusion, although it can by no means confirm a diagnosis of pericarditis. Significant fluid collection in the pericardial space may cause the heart to appear larger than normal—or larger than on an earlier chest film—and raises suspicions of pericarditis. A large effusion can appear as a classic "water-bottle" heart. Imaging methods, especially echocardiography, are usually definitive.

Serial chest films can demonstrate a progressive decrease in heart size if constrictive pericarditis develops as an effusion is absorbed. Patients with constrictive pericarditis have normal or enlarged cardiac silhouettes (see the image). The formation of fibrinous exudates within the pericardial space, caused by pericarditis, can lead to the development of constrictive pericarditis. This thickening and scarring of the pericardium can eventually prevent normal diastolic filling. Constrictive pericarditis following shortly after acute pericarditis is often transient and does not require pericardiectomy. It responds quickly to NSAID treatment.

WHAT THE ECG MAY REVEAL

A diagnosis of pericarditis is easily overlooked if the symptoms are atypical, especially if a pericardial rub is absent or the pain resembles angina, chest wall pain, or muscular pain. An ECG is indicated in any patient with significant chest pain. Characteristic ECG findings in acute pericarditis are tachycardia and widespread ST-segment elevation. Elevation in 6 or more leads, including the inferior and anterior leads, and widespread elevation in leads V₂ through V₆ are typical in patients with acute pericarditis. Diffuse, concave ST-segment elevation is characteristic of pericarditis; convex ST-segment elevation is more typical of MI.

ST-segment elevation in both the inferior and anterior leads is unusual in a patient having an MI; a more common finding in MI would be elevation on one side and a reciprocal depression on the other. Lack of reciprocal ST-segment changes can help differentiate acute pericarditis from MI. Typically, the only leads that nearly always demonstrate ST-segment depression in patients with acute pericarditis are aVR and V₁—rarely V₂.

Depression of the PR segment is very specific for pericarditis and occurs in all leads except aVR and V₁, in which reciprocal elevation may be seen. In fact, the sooner patients with pericarditis present after the onset of chest pain, the more likely that PR-segment depression will be the only ECG abnormality. Slightly later in the course of the disease, both ST-segment elevation and PR-segment depression appear, and subsequently, the PR-segment depression may return to normal, while the ST-segment elevation remains. In a patient who presents several days after symptoms of pericarditis appear, the ECG may have evolved, losing its classic diffuse ST-segment elevation and taking on the appearance of an ECG more consistent with diffuse myocarditis or ischemia—or the ECG may be normal. Rapid return to normal is increasingly frequent, probably due to effective anti-inflammatory therapy.

Abnormal Q waves are diagnostic of MI and cannot be attributed to pericarditis. Bradycardia is rarely seen in patients with acute pericarditis. T-wave inversion in the leads showing ST-segment depression is associated with MI. In the very early stages of infarction, however, ST-segment elevation with an upright T wave often occurs; the T wave will begin to invert before the ST segment returns toward the baseline. In pericarditis, the T wave remains upright even when the ST segment is elevated, and T-wave inversion, when it occurs, does not do so until after the ST segment returns to baseline.

Serial ECGs can prove helpful in differentiating pericarditis from infarction. If a subsequent ECG shows Q waves that were not present on the initial tracing or T waves that are beginning to invert while the ST segments remain elevated, a diagnosis of MI is more likely. Large increases in cardiac enzyme levels support a diagnosis of infarction.

Diagnosing acute pericarditis often requires a good deal of clinical judgment. As many as half of patients who have acute pericarditis will not present with typical ECG findings. Note whether the patient reports less pain when sitting up or leaning forward. Listen repeatedly for a pericardial rub. If a patient has minimal risk factors for ischemic heart disease and the pain is influenced by posture and respiration, acute pericarditis should be a leading candidate in the differential diagnosis.

COMPLICATIONS: EFFUSION AND CARDIAC TAMPONADE

The pericardium, which helps maintain cardiac shape, position, and function, consists of 2 layers: the visceral pericardium and the parietal pericardium. The space between these 2 layers contains 10 to 35 mL of fluid under normal conditions, which helps protect the heart and maintain a stable pressure within the pericardium throughout respiration and postural changes. Injury, infection, and other conditions can trigger an inflammatory response and the accumulation of excess pericardial fluid. Pericardial effusion is always a danger in any patient with pericarditis.

Depending on how much and how quickly fluid accumulates in the pericardial space, hemodynamic compromise or cardiac tamponade can result. If a large amount of fluid accumulates quickly, the pericardium cannot stretch to accommodate the added volume. The fluid compresses the heart, compromising diastolic filling and causing a decline in arterial pressure. In cardiac tamponade, competition between the left and right sides of the heart in a fixed pericardial space is the major cause of physically reduced aortic flow and pressure during inspiration (pulsus paradoxus). Cardiac tamponade accompanying pericarditis occurs most often in the setting of chest trauma, after cardiac surgery, and when there is neoplastic involvement of the pericardium. Pericardiocentesis is the definitive treatment. Analysis of the aspirated fluid may provide evidence of an infectious or neoplastic etiology.

Pulsus paradoxus is an important clinical feature of severe cardiac tamponade, yet it is not diagnostic for that condition. It occurs very infrequently in patients with constrictive pericarditis, shock, pulmonary embolism, asthma, and tension pneumothorax associated with severe obstructive airway disease.

Evidence of excessive fluid in the pericardial space supports a diagnosis of pericarditis, but its absence does not rule out pericarditis. Furthermore, excess pericardial fluid can be present without pericarditis. Patients with congestive heart failure and kidney disease, for example, and women in the third trimester of pregnancy tend to retain fluid, which can lead to increased fluid volume in the pericardial space.

Echocardiography is a helpful component of the diagnostic workup but should not be relied on as a diagnostic indicator of acute pericarditis. In a litigious environment, though, it might be wise to check for an effusion since cardiac tamponade is the riskiest complication in patients with acute pericarditis. Echocardiography can confirm an effusion, demonstrate the amount of fluid present, and show chamber collapses, which are highly suggestive of cardiac tamponade. It can also help rule out other cardiac disorders, such as endocarditis. Confirmation of an effusion contraindicates thrombolytic therapy in suspected MI.

Echocardiography, when it discloses even a small effusion, can be helpful in confirming the diagnosis. The use of echocardiography for the evaluation of all patients with suspected pericardial disease is recommended by the American College of Cardiology, the American Heart Association, and the American Society of Echocardiography.

RECURRENT PERICARDITIS

A very troublesome complication of acute pericarditis is recurrence in 15% to 30% of cases. The principles of treatment are the same as those for simple acute pericarditis: avoid corticosteroids whenever possible, relying instead on NSAIDs. Colchicine has been shown to reduce the frequency of recurrence by more than two thirds and to decrease the severity. Colchicine also shortens the course of acute pericarditis when added to NSAID treatment.

RELIEVING THE PAIN AND REDUCING THE INFLAMMATION

Patients who have acute pericarditis are often in a great deal of persistent pain. To reduce the inflammation and ease the pain, NSAIDs including salicylates are recommended. Indomethacin (Indocin) should not be used in elderly patients because it may cause decreased coronary flow by inducing coronary spasm.

Patient positioning can also relieve the discomfort. In rare instances, morphine or several days of tapered corticosteroid therapy may be considered if pain is intractable. If possible, treat the underlying cause of the pericarditis. This would include antibiotic therapy in cases of bacterial pericarditis, as shown by Gram's stain and culture of the pericardial fluid.

Colchicine has proved effective, usually with an NSAID, but even as monotherapy. Pretreatment with a corticosteroid will diminish colchicine's effectiveness and promote recurrent acute pericarditis. Colchicine also reduces recurrences.

Patients also need reassurance that they are not having a heart attack and that this disturbing episode will resolve shortly. Continue to monitor for atrial or supraventricular arrhythmias and for signs of heart failure. The pain of pericarditis treated with NSAIDs should typically resolve within a day or two.

This article was updated in consultation with Drs Marinella, Shabetai, and Spodick and edited by Deborah Kaplan.

Drs Marinella, Shabetai, and Spodick disclose that they have no financial relationship with any manufacturer in this area of medicine.

SUGGESTED READING

Adler Y, Finkelstein Y, Guindo J, et al. Colchicine treatment for recurrent pericarditis: a decade of experience. Circulation. 1998;97:2183-2185.

ESC Task Force. Guidelines on the diagnosis and management of pericardial diseases. EurHeart J. 2004;25:587-610.

Farraj RS, McCully RB, Oh JK, et al. Mycoplasma-associated pericarditis. Mayo Clin Proc. 1997;72:33-36.

Gosselink AT, van den Berg MP, Crijns HJ. Acute pericarditis presenting with sinus bradycardia: a case report. Int J Cardiol. 1997;60:307-310.

Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005;112:2012-2016.

Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. 2003;42:2144-2148.

Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol. 2004;43:1042-1046.

Marinella MA. Electrocardiographic manifestations and differential diagnosis of acute pericarditis. Am Fam Physician. 1998;57:699-704.

Saenz RE, Sanders CV, Aldridge KE, et al. Purulent pericarditis with associated cardiac tamponade caused by a Streptococcus pneumoniae strain highly resistant to penicillin, cefotaxime, and ceftriaxone. Clin Infect Dis. 1998;26:762-763.

Sinha PR, Singh BP, Jaipuria N, et al. Intrapericardial echogenic images and development of constrictive pericarditis in patients with pericardial effusion. Am Heart J. 1996;132:1268-1272.

Spodick DH. The Pericardium: A Comprehensive Textbook. New York, NY: Marcel Dekker; 1997.

Zales VR, Wright KL. Endocarditis, pericarditis, and myocarditis. Pediatr Ann. 1997;26:116-121.

Acute pericarditis symptom management

• Restrict exercise.
• Manage pain.
• When the diagnosis of uncomplicated acute pericarditis is obvious, hospital admission is unnecessary. The patient can be monitored and treated in a day care or clinic setting.
• When complicated acute pericarditis is suspected (large effusion, suspicion of cardiac tamponade, failure of NSAIDs to produce prompt relief), the patient must be hospitalized for diagnostic testing to determine the etiology of the pericarditis.