ECG Changes in Pericarditis
A 26-year-old otherwise healthy man presents to the emergency department with a 3- to 4-hour history of left-sided chest pain. The pain is pleuritic and accompanied by nausea and discomfort in the left arm. The patient denies dyspnea, diaphoresis, fever, chills, headache, diarrhea, leg swelling, and myalgia. There is no recent history of upper respiratory tract infection, contact with ill persons, or trauma.
History. The patient had an episode of pericarditis 1 year earlier. At that time, he had similar chest pain and was admitted for observation. Cardiac markers were negative for myocardial infarction (MI). An echocardiogram revealed normal wall motion and valves and no pericardial effusion. NSAID therapy was prescribed. The patient was discharged home and had no further pain.
The patient is a smoker, but denies alcohol and illicit drug use. He uses no daily medications or supplements. His father died at age 39 years of an unknown cardiac condition.
Examination. The patient is in no acute distress. His temperature is 36.3º C (97.3°F); blood pressure, 116/69 mm Hg; respiration rate, 14 breaths per minute; heart rate, 66 beats per minute; and oxygen saturation, 99% on room air. Heart rate and rhythm are regular with no murmurs or gallops, no muffled heart sounds, and no reproducible chest pain. When the patient is asked to lean forward, an intermittent pericardial friction rub is audible. The lungs are clear to auscultation; there is no jugular venous distention, no carotid bruit, and no lower extremity edema. The remainder of the examination is unremarkable.
Diagnostic studies. An ECG shows sinus bradycardia with diffuse ST-T wave elevation (Figure). The tracing is identical to the one taken a year ago. The troponin concentration obtained in triage is normal.
Outcome. The patient is discharged home with a diagnosis of recurrent pericarditis and a prescription for NSAIDs. In the disposition, the examiners considered his relatively good examination results, which included no signs of toxicity, distress, or heart failure. At the time of his previous episode, he was thoroughly evaluated for cardiac disease, tuberculosis, and connective tissue disorders.
PERICARDITIS: AN OVERVIEW
Pericarditis, an inflammatory process within the pericardial sac, may or may not be associated with a pericardial effusion. Causes include viral or bacterial infection; post-MI status (Dressler pericarditis), chest trauma, metabolic disorder (uremia, hypothyroidism), malignancy, radiation, and collagen vascular disease. Drug-induced systemic lupus erythematosus may also produce pericarditis; the culprit agents include hydralazine, procainamide, and isoniazid. Most of these causes can induce both "dry" pericarditis and pericardial effusive disease, or "wet" pericarditis.
The most common causes of acute pericarditis are either viral or idiopathic (Table).1 When the cause is believed to be viral, a pathogen is recovered in only 20% to 30% of cases.2 Common viral culprits include coxsackieviruses, echoviruses, adenoviruses, Epstein-Barr virus, and influenza viruses. Other infectious causes are Mycobacterium tuberculosis, staphylococci, Haemophilus organisms, pneumococci, Salmonella organisms, meningococci, Treponema pallidum, Rickettsia rickettsii, Chlamydia psittaci, Borrelia burgdorferi, actinomycetes, Mycoplasma pneumoniae, Nocardia organisms, and fungi.
The classic presentation of pericarditis is chest pain that worsens in the supine position and is relieved in the sitting position. The pain may radiate to the ridge of the trapezius, a sign that is highly specific for pericardial inflammation.3 Tachycardia is common. Other findings include fatigue, tachypnea, neck vein distention, pulsus paradoxus, hepatomegaly, lower extremity edema, and thready distal pulses if heart failure is present.
The cardiac auscultatory findings include a harsh-sounding friction rub or muffled heart tones, which correlate with fluid in the pericardial sac. The pericardial friction rub, if present, is best heard when the patient sits up and leans forward. The friction rub of pericarditis can be distinguished from a pleural friction rub by having the patient hold his or her breath during auscultation. The pleural rub cannot be heard when respiration is suspended.
ECG changes typically occur in 4 stages1:
- Stage 1 is characterized by diffuse upward concave ST-segment elevation with concordance of T waves, ST-segment depression in aVR or V1, and low voltage. The PR-segment depression is usually seen in the leads with ST-segment elevations.
- Stage 2: ST segments return toward baseline with flattening of the T waves.
- Stage 3: T-wave inversion.
- Stage 4: Gradual resolution and return to baseline.
Pericarditis is a clinical diagnosis supplemented by ECG findings. The erythrocyte sedimentation rate is usually elevated, but this value does not need to be obtained to make the diagnosis. Echocardiography may be used to exclude pericardial effusion and structural abnormalities.
Pain control is the mainstay of treatment. If a specific bacterial cause is identified, antibiotic therapy is initiated.4 Aggressive pain control may be necessary in some patients, although most respond to salicylates or NSAIDs.
Corticosteroid therapy is rarely indicated. Consider this option only when NSAIDs are ineffective and a bacterial cause has clearly been excluded.4
Emergency pericardiocentesis is required for all patients with clinical evidence of cardiac tamponade, suspected bacterial pericarditis, and imminent decompensation. Nonemergent pericardiocentesis is useful as a diagnostic test in patients with a pericardial effusion of unknown cause and is usually performed under ultrasound guidance. Any fluid aspirated from the pericardial space should be sent for routine cell counts, Gram staining, cultures, and protein level.
Recurrent episodes of pericarditis occur in 15% to 32% of patients; the cause is thought to be idiopathic.5 Colchicine may reduce the likelihood of a recurrence; it has been effective in treating both initial and recurrent episodes.5,6 The exact mechanism of action is unclear, but colchicine acts as an anti-inflammatory agent in pericarditis. The recommended dosage for a recurrent episode is 1 mg/d for at least 1 year, with gradual tapering.5 Some sources recommend using colchicine before a trial of corticosteroids.
Almost all patients recover completely if no serious acute complication occurs. Most healthy young patients can be managed on an outpatient basis with good follow-up.
Hospitalize patients with any of the following poor prognostic indicators: fever, subacute onset, immunosuppressed states, pericarditis from trauma, a history of anticoagulant therapy, large pericardial effusion, or cardiac tamponade.1
This patient was discharged home with ibuprofen and was to be seen again in 3 to 5 days. However, he did not make an outpatient appointment and was lost to follow-up.
1. Lange RA, Hills LD. Acute pericarditis. N Engl J Med. 2004;351:2195-2202.
2. Gewitz MH, Vetter V. Cardiac emergencies. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 4th ed. Baltimore: Lippincott Williams & Wilkins; 2000:659-700.
3.Spodick DH. Acute pericarditis, current concepts and practice. JAMA. 2003;289:1150-1153.
4. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; The Task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J. 2004;25:587-610.
5. Adler Y, Finkelstein Y, Guindo J, et al. Colchicine treatment for recurrent pericarditis: a decade of experience. Circulation. 1998;97:2183-2185.
6. Millaire A, DeGroote P, Decoulx E, et al. Treatment of recurrent pericarditis with colchicine. Eur Heart J. 1994;15:120-124.