Definition and epidemiology
Pericarditis is inflammation of the pericardium, the fibroserous sac surrounding the heart, often accompanied by a pericardial effusion. It is the most common disease affecting the pericardium and a frequent cause of chest pain evaluated in emergency settings.
- Accounts for roughly 5% of emergency department visits for non-ischemic chest pain
- Most common in adults 20-50 years old, with a male predominance
- Idiopathic/presumed viral etiology accounts for the majority of cases in developed countries
- Tuberculous pericarditis remains an important cause in regions with high TB prevalence and in HIV-positive patients
Pericarditis is classified by duration: acute (new onset, less than 4-6 weeks), incessant (lasting beyond 4-6 weeks but less than 3 months), recurrent (relapse after a symptom-free interval of at least 4-6 weeks), and chronic (lasting more than 3 months).
- Chest pain improves on leaning forward, worsens lying supine - classic for pericarditis
- ECG shows diffuse ST elevation with PR depression, PR elevation in aVR
- Diagnosis needs 2 of 4: pain, rub, ECG changes, new effusion
- First-line treatment is NSAID or aspirin plus colchicine
- Colchicine reduces recurrence risk - add in all patients without contraindication
- Avoid NSAIDs (other than aspirin) in post-MI pericarditis to protect infarct healing
- Dressler syndrome = pericarditis weeks after MI, autoimmune mechanism
- Early corticosteroid use increases risk of recurrent pericarditis
Etiology and risk factors
Infectious causes
- Viral (most common identified cause): coxsackievirus, echovirus, adenovirus, influenza, and others
- Bacterial (purulent pericarditis): less common, more severe
- Tuberculous: important worldwide, especially with HIV coinfection
Non-infectious causes
- Idiopathic: largest single category, likely many are unrecognized viral cases
- Autoimmune/connective tissue disease: systemic lupus erythematosus, rheumatoid arthritis, scleroderma
- Post-myocardial infarction: early (peri-infarction) or late (Dressler syndrome, typically weeks after MI)
- Uremic pericarditis: in advanced chronic kidney disease
- Malignancy: metastatic disease (lung, breast), lymphoma
- Post-cardiac injury syndrome: after cardiac surgery, trauma, or percutaneous procedures
- Drug-induced: hydralazine, procainamide, isoniazid
- Radiation-induced: prior mediastinal radiotherapy
- Metabolic: hypothyroidism
Pathophysiology
Inflammation of the pericardial layers (visceral and parietal) leads to irritation of pain-sensitive fibers, most densely located in the lower parietal pericardium and diaphragmatic surface, which explains referral of pain to the trapezius ridge via the phrenic nerve.
Inflammatory exudate can accumulate between the layers, producing a pericardial effusion. If fluid accumulates rapidly or in large volume, intrapericardial pressure rises and can impair diastolic filling of the heart, producing cardiac tamponade, a medical emergency.
Repeated or chronic inflammation can lead to pericardial fibrosis and calcification, resulting in constrictive pericarditis, in which a rigid, non-compliant pericardium restricts ventricular filling.
Clinical features
- Chest pain: sharp, pleuritic, retrosternal or left-sided; classically worsens with inspiration, coughing, and lying supine, and improves with sitting up and leaning forward
- Pain may radiate to the trapezius ridge (relatively specific for pericarditis)
- Low-grade fever, malaise, and a preceding viral prodrome are common
- Pericardial friction rub: scratchy, high-pitched sound best heard at the left sternal border with the patient leaning forward, classically has up to three components (atrial systole, ventricular systole, ventricular diastole)
- Dyspnea if a significant effusion is present
- Signs of tamponade (if present): hypotension, elevated jugular venous pressure, muffled heart sounds (Beck triad), pulsus paradoxus
Diagnosis
Diagnosis requires at least 2 of 4 clinical criteria:
- Characteristic pleuritic chest pain
- Pericardial friction rub
- New widespread ST elevation or PR depression on ECG
- New or worsening pericardial effusion
ECG
- Diffuse concave ("saddle-shaped") ST elevation and PR segment depression, typically sparing lead aVR (which shows PR elevation)
- Evolves through four stages but changes are often less predictable than textbook description
Laboratory and imaging
- Elevated inflammatory markers (CRP, ESR) support diagnosis and help monitor response to treatment
- Troponin may be mildly elevated if there is associated myocarditis (myopericarditis)
- Echocardiography: recommended in all patients to assess for effusion and tamponade physiology
- Chest X-ray: usually normal unless large effusion ("water bottle" cardiac silhouette) or underlying pulmonary disease
- Cardiac MRI: useful for detecting pericardial inflammation/edema in equivocal or recurrent cases
- Further workup (ANA, rheumatoid factor, TB testing, blood cultures) guided by clinical suspicion of secondary cause
Differential diagnosis
| Condition | Distinguishing feature |
|---|---|
| Acute myocardial infarction | Localized ST elevation with reciprocal changes, troponin rise pattern, regional wall motion abnormality |
| Myocarditis | Overlaps with pericarditis (myopericarditis); more prominent troponin elevation, possible arrhythmia or heart failure |
| Pulmonary embolism | Pleuritic pain with dyspnea, tachycardia, risk factors for VTE, normal ECG findings different (sinus tachycardia, S1Q3T3) |
| Aortic dissection | Tearing pain radiating to back, pulse/blood pressure differential between limbs |
| Pneumonia/pleuritis | Fever, productive cough, consolidation on imaging |
| Costochondritis | Reproducible chest wall tenderness on palpation, no systemic or ECG findings |
| GERD | Burning, related to meals/position, responds to antacids |
Management
Most cases of acute idiopathic/viral pericarditis are managed empirically and respond well to anti-inflammatory therapy. Identify and treat any specific underlying cause (e.g., dialysis for uremic pericarditis, antituberculous therapy for TB).
First-line therapy
- NSAIDs (e.g., ibuprofen, indomethacin) or aspirin (preferred in post-MI pericarditis, since other NSAIDs may impair infarct healing)
- Colchicine added to NSAID/aspirin therapy in all patients without contraindication, as it reduces symptom duration and significantly lowers the risk of recurrence
- Treatment is typically continued for 1-2 weeks with gradual tapering guided by symptoms and CRP normalization rather than fixed duration alone
Additional measures
- Restriction of strenuous physical activity until symptom resolution and normalization of inflammatory markers
- Corticosteroids: reserved for cases refractory to NSAIDs/colchicine, contraindications to NSAIDs, or specific autoimmune etiologies; use is discouraged as first-line because it increases recurrence risk
- Recurrent/refractory pericarditis: steroid-sparing agents (e.g., azathioprine, IV immunoglobulin) or IL-1 blockade (e.g., anakinra, rilonacept) in specialist-managed cases
Specific situations
- Cardiac tamponade: urgent pericardiocentesis
- Purulent bacterial pericarditis: antibiotics plus pericardial drainage
- Chronic constrictive pericarditis: pericardiectomy if symptomatic and refractory to medical therapy
Guideline consensus (ESC and widely adopted in US practice) supports NSAID/aspirin plus colchicine as first-line for acute pericarditis; routine corticosteroid use as initial therapy is discouraged across major guidelines.
Complications and prognosis
- Cardiac tamponade: most feared acute complication, requires emergent drainage
- Recurrent pericarditis: occurs in roughly 20-30% after a first episode, especially if colchicine was not used or corticosteroids were used early
- Constrictive pericarditis: uncommon long-term complication, more frequent after tuberculous, purulent, or post-surgical pericarditis
- Myopericarditis: concurrent myocardial involvement, usually self-limited but warrants activity restriction and monitoring
Overall prognosis for idiopathic/viral acute pericarditis is excellent with appropriate therapy; most patients recover fully without long-term sequelae. Prognosis is less favorable with purulent, tuberculous, or malignancy-related pericarditis, which depends on the underlying cause.
PERICARDITIS causes - CARDIAC RIND: Collagen vascular disease, Aortic aneurysm (dissection), Radiation, Infections, Drugs, Acute renal failure (uremia), Cardiac infarction (Dressler), Rheumatic fever, Injury, Neoplasm, iDiopathic
Practice questions
1. A 28-year-old man presents with 2 days of sharp substernal chest pain that worsens when he lies down and improves when he sits forward. He had an upper respiratory infection last week. Temperature is 37.8°C. A scratchy sound is heard at the left sternal border. ECG shows diffuse ST elevation with PR depression. Which of the following is the most appropriate initial treatment?
2. A 60-year-old woman develops recurrent chest pain and a new pericardial friction rub six weeks after an anterior ST-elevation myocardial infarction treated with primary angioplasty. She is afebrile and hemodynamically stable. Which of the following best describes this condition?
3. A 55-year-old man with pericarditis develops progressive dyspnea, hypotension, and distended neck veins. On exam, heart sounds are faint and there is a drop in systolic blood pressure of 15 mmHg during inspiration. Echocardiography shows a large pericardial effusion with right ventricular diastolic collapse. What is the most appropriate next step?
Frequently asked questions
What causes pericarditis?
The most common identifiable cause is viral infection, and many idiopathic cases are presumed viral as well. Other causes include autoimmune disease, uremia from kidney failure, post-myocardial infarction (Dressler syndrome), malignancy, tuberculosis, certain drugs, and prior chest radiation or cardiac surgery.
What are the first symptoms of pericarditis?
The hallmark first symptom is sharp, pleuritic chest pain that worsens with lying flat, coughing, or deep breathing and improves when sitting up and leaning forward. It is often preceded by a viral illness with low-grade fever and malaise, and pain may radiate to the shoulder or trapezius ridge.
How is pericarditis diagnosed?
Pericarditis is diagnosed clinically using criteria requiring at least two of: characteristic chest pain, a pericardial friction rub on exam, diffuse ST elevation or PR depression on ECG, or a new pericardial effusion on echocardiography. Blood tests for inflammatory markers and echocardiography are routinely obtained to support diagnosis and assess severity.
Is pericarditis curable?
Yes, most cases of acute idiopathic or viral pericarditis resolve completely with NSAID and colchicine therapy within days to a couple of weeks. However, roughly 20-30% of patients experience at least one recurrence, and a small subset develop chronic or constrictive disease requiring longer-term management.
Pericarditis vs myocardial infarction - what is the difference?
Pericarditis causes diffuse, concave ST elevation across most ECG leads with PR depression and pain that changes with position, while MI causes localized ST elevation in a specific coronary territory with reciprocal depression and pain unaffected by posture. Troponin and wall motion abnormalities also help distinguish ongoing infarction from pericarditis.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: I32
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.