Emergency Department Workup for Suspected Acute Pericarditis
Obtain a 12-lead ECG within 10 minutes and measure high-sensitivity cardiac troponin immediately—even when pericarditis is suspected—because acute coronary syndrome must be excluded first, and up to 13% of patients with pleuritic chest pain have myocardial ischemia. 1, 2
Immediate Diagnostic Actions (First 10 Minutes)
Acquire and interpret a 12-lead ECG within 10 minutes to identify STEMI, ST-depression, T-wave inversions, or the classic pericarditis pattern of diffuse concave ST-elevation with PR-segment depression. 1, 3
Draw high-sensitivity cardiac troponin immediately because it is the most sensitive and specific biomarker for myocardial injury; troponin can be mildly elevated in myopericarditis but markedly elevated troponin suggests STEMI or NSTEMI. 1, 3, 4
Measure vital signs promptly (heart rate, bilateral arm blood pressures, respiratory rate, oxygen saturation) to detect hemodynamic instability, pulse differentials suggesting aortic dissection, or tachycardia/tachypnea indicating pulmonary embolism. 1, 2
Perform a focused cardiovascular examination for pericardial friction rub (present in <30% of acute pericarditis but highly specific when found), new murmurs, S3 gallop, jugular venous distension, unilateral absent breath sounds, and signs of tamponade. 1, 2, 5, 6
Clinical Features Supporting Pericarditis
Sharp, pleuritic chest pain that worsens when lying supine and improves when sitting forward or leaning forward is the hallmark presentation, occurring in approximately 90% of acute pericarditis cases. 1, 2, 5, 6
Pain that increases with deep breathing, coughing, or swallowing further supports pericarditis over myocardial ischemia. 2, 6
A pericardial friction rub is pathognomonic when present but is heard in fewer than 30% of cases; its absence does not exclude pericarditis. 1, 2, 5, 6
Fever commonly accompanies acute pericarditis, particularly in viral or idiopathic cases. 1, 2, 6
Electrocardiographic Findings in Pericarditis
Diffuse concave upward ST-segment elevation without reciprocal ST-depression or Q waves is the classic ECG pattern, present in 25–50% of acute pericarditis cases. 1, 5, 6
PR-segment depression (best seen in leads II, aVF, and V4–V6) is highly specific for pericarditis when present alongside ST-elevation. 1, 5, 6
Absence of reciprocal ST-depression distinguishes pericarditis from STEMI; STEMI typically shows reciprocal changes in opposite leads. 1, 6
Life-Threatening Conditions That Must Be Excluded First
Acute Coronary Syndrome
- Retrosternal pressure, squeezing, or heaviness that builds over minutes and radiates to the left arm, jaw, or neck is typical of ACS, not pericarditis. 1, 2
- Approximately 13% of patients with pleuritic-type chest pain still have acute myocardial ischemia, so pleuritic features do not rule out ACS. 1, 2
- A normal physical examination does not exclude uncomplicated myocardial infarction. 1, 2
Aortic Dissection
- Sudden "ripping" or "tearing" chest or back pain maximal at onset, pulse differential between extremities (≈30% of cases), or systolic blood pressure difference >20 mmHg between arms suggests dissection. 1, 2
Pulmonary Embolism
- Sudden dyspnea with pleuritic chest pain, tachycardia (>90% of PE patients), and tachypnea are hallmarks of PE. 1, 2
Cardiac Tamponade
- Jugular venous distension, hypotension, muffled heart sounds (Beck's triad), and pulsus paradoxus >10 mmHg indicate tamponade requiring urgent pericardiocentesis. 7, 1, 8
Additional Diagnostic Testing
Obtain a chest radiograph to evaluate for cardiomegaly (suggesting large pericardial effusion), pneumothorax, pneumonia, or widened mediastinum (aortic dissection). 3, 9
Perform bedside transthoracic echocardiography to detect pericardial effusion (present in ≈60% of acute pericarditis), assess for tamponade physiology, evaluate regional wall motion abnormalities (suggesting myocardial ischemia), and exclude aortic dissection. 7, 1, 8, 5
Measure C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) as markers of inflammation; elevated levels support pericarditis and guide treatment duration. 8, 5
Check complete blood count, renal function, and thyroid-stimulating hormone to identify systemic causes (uremia, hypothyroidism, autoimmune disease). 8, 6
Risk Stratification for Pericarditis
High-risk features requiring hospital admission and cardiology consultation include: 8, 5, 6
- Fever >38°C (100.4°F)
- Subacute onset over days to weeks (suggesting tuberculous or neoplastic etiology)
- Large pericardial effusion (>20 mm echo-free space in diastole)
- Cardiac tamponade
- Failure to respond to NSAIDs after 7 days
- Myopericarditis (troponin elevation with regional wall motion abnormalities)
- Immunosuppression
- Trauma
- Oral anticoagulant therapy
Low-risk patients (young, otherwise healthy, no high-risk features, small or no effusion) can be managed as outpatients with close follow-up. 5, 6
Initial Management in the Emergency Department
Administer high-dose NSAIDs as first-line therapy: ibuprofen 600–800 mg three times daily or indomethacin 50 mg three times daily, tapered over several weeks once chest pain resolves and CRP normalizes. 8, 5, 6
Add colchicine 0.6 mg twice daily (or 0.6 mg once daily if <70 kg) for 3 months to relieve symptoms and reduce recurrence risk from 37.5% to 16.7% (absolute risk reduction 20.8%). 8, 5, 6
Provide gastroprotection with a proton-pump inhibitor when using NSAIDs. 8, 6
Avoid corticosteroids as initial therapy because they increase the risk of recurrence; reserve them for refractory cases, contraindications to NSAIDs, or immune-mediated etiologies (connective tissue disease, uremia). 8, 5, 6
Restrict physical activity (no strenuous exercise or competitive sports) until symptoms resolve and CRP normalizes, typically 3 months for athletes. 5, 6
Common Pitfalls to Avoid
Do not rely on nitroglycerin response to differentiate pericarditis from ACS; esophageal spasm and other conditions also respond to nitroglycerin. 1, 2
Do not dismiss ACS solely because pain is pleuritic or positional; 13% of patients with pleuritic pain have myocardial ischemia. 1, 2
Do not assume a normal ECG excludes ACS; 30–40% of acute myocardial infarctions present with a normal or nondiagnostic initial ECG. 1
Do not delay transfer to the ED for troponin testing in office settings when ACS or pericarditis is suspected; arrange urgent EMS transport. 1, 3
Do not use corticosteroids as first-line therapy unless NSAIDs are contraindicated; steroids increase recurrence rates. 8, 5, 6
Disposition Algorithm
If ECG shows STEMI or troponin is markedly elevated → Activate STEMI protocol, treat as acute coronary syndrome. 1, 3
If clinical features suggest tamponade (hypotension, jugular venous distension, pulsus paradoxus) → Perform urgent pericardiocentesis. 7, 8
If high-risk features are present → Admit for inpatient monitoring, cardiology consultation, and further workup (tuberculosis testing in endemic areas, autoimmune serologies, viral titers). 8, 5, 6
If low-risk pericarditis is confirmed → Discharge with NSAIDs, colchicine, gastroprotection, activity restriction, and outpatient cardiology follow-up in 1 week to reassess symptoms and repeat CRP. 5, 6