Pericarditis

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pericarditis ECG saddle-shaped ST elevation

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Pericarditis

Definition & Epidemiology

Pericarditis is inflammation of the pericardium caused by granulocytic and lymphocytic infiltration. It accounts for approximately 5% of all non-ischemic chest pain in the emergency setting. In Western countries, 80–90% of cases are labeled idiopathic, though most are presumed viral. Tuberculosis is a leading cause in developing countries.
Rosen's Emergency Medicine, p. 1121

Etiology

CategoryExamples
InfectiousViral (coxsackievirus, echovirus, adenovirus, EBV, influenza), bacterial (pneumococcus, S. aureus, meningococcus, H. influenzae), fungal, parasitic
Post-injury / IatrogenicPost-MI (Dressler syndrome), post-pericardiotomy, blunt/penetrating trauma, radiation, cardiac procedures
Systemic / AutoimmuneSLE, RA, systemic sclerosis, sarcoidosis, amyloidosis
MetabolicUremia
NeoplasticMetastatic tumors, primary tumors
Drug-inducedVarious agents (see recent 2026 systematic review, PMID 41276190)
A specific viral agent is recovered in only 20–30% of viral cases; no cause is established in up to 55% of patients in comprehensive studies.

Pathophysiology

The pericardium consists of parietal and visceral layers (each 1–2 mm), with a 15–35 mL ultrafiltrate normally present in the pericardial space. Its functions include maintaining cardiac position, preventing infection spread, and maintaining normal pressure-volume relationships. Inflammation leads to increased antibodies in pericardial fluid; recent research distinguishes autoinflammatory vs. autoimmune pericarditis.

Clinical Features

Symptoms

  • Chest pain: sharp, pleuritic, retrosternal — the cardinal symptom
    • Worsened by lying supine, deep inspiration, swallowing
    • Relieved by sitting forward (orthopnea characteristic)
    • Can radiate to trapezius muscles, back, or present as isolated shoulder pain
  • Fever, myalgias, dyspnea (may have pleuritic component)

Signs

  • Pericardial friction rub — pathognomonic
    • Best heard: lower left sternal border, diaphragm of stethoscope, patient leaning forward in full expiration
    • Has up to 3 components (ventricular systole, early diastolic filling, atrial systole)
    • Tends to be intermittent and migratory

Diagnosis

No single test is diagnostic. The diagnosis requires ≥2 of 4 criteria:
  1. Typical chest pain
  2. Pericardial friction rub
  3. ECG changes
  4. New/worsening pericardial effusion
Classic pain + ECG pattern seen in only ~two-thirds of patients.

ECG Changes (4 Stages)

StageTimingFindings
1Hours–daysDiffuse concave (saddle-shaped) ST elevation, reciprocal ST depression in aVR, PR depression in most leads, PR elevation in aVR
2DaysST and PR segments normalize
3Days–weeksT-wave flattening → deep, symmetrical T-wave inversions
4WeeksECG returns to normal (T-wave inversions may persist)
Key ECG distinguishing features from STEMI:
  • ST elevation is concave (not convex)
  • Diffuse distribution (not single coronary territory)
  • No simultaneous T-wave inversion with ST elevation
  • No Q waves develop
  • PR depression is highly specific for pericarditis (Spodick's sign = down-sloping TP segments)
12-lead ECG showing classic acute pericarditis: diffuse saddle-shaped ST elevation, PR depression in II and lateral leads, reciprocal changes in aVR
Classic 12-lead ECG of acute pericarditis: diffuse concave ST elevation, PR depression (most visible in II), PR elevation in aVR, and Spodick's sign. Note the non-territorial distribution distinguishing it from STEMI.

Other Investigations

  • Echocardiography: effusion in up to 60% (POCUS); normal echo does not exclude pericarditis
  • CRP: elevated in inflammation; useful for monitoring treatment response
  • CBC, ESR: not sensitive or specific
  • Troponin: elevated in ~35% if concurrent myopericarditis
  • Cardiac MRI: pericardial delayed hyperenhancement confirms ongoing inflammation; defines extent of involvement
  • Pericardial fluid analysis: rarely useful unless infective pericarditis is suspected

Management

Acute Pericarditis

First-line (NSAIDs ± Colchicine):
  • Ibuprofen 600 mg QID × 10 days or
  • Indomethacin 25 mg TID or
  • Aspirin 650 mg TID × 10 days
  • If initial NSAID fails within 1 week, switch NSAID class (e.g., naproxen 250 mg BID × 7 days)
Colchicine (add to NSAIDs):
  • Reduces recurrence rate by ~50% (COPE trial)
  • Weight ≥70 kg: 0.5–0.6 mg BID; weight <70 kg: 0.5 mg once daily
  • Duration: 3–6 months
  • Caution: renal failure, pregnancy
  • Start in the ED for best outcomes
Second-line (Corticosteroids):
  • Reserved for: failure of NSAIDs/aspirin, contraindication to NSAIDs, anticoagulant use
  • Low-to-moderate dose preferred: prednisone 0.2–0.5 mg/kg/day (lower recurrence than 1 mg/kg/day)
Refractory / Recurrent Pericarditis:
  • Anakinra (IL-1β receptor antagonist) — promising in colchicine-refractory or steroid-dependent cases
  • Azathioprine, IVIG — limited evidence
  • Pericardiectomy — last resort

Disposition

Indication for HospitalizationDetails
Hemodynamic abnormalityTamponade physiology
Temperature >38°C / 100.4°FHigh-risk feature
Large effusionRisk of tamponade
Failure of first-round treatment
Diagnostic uncertainty with ACSRule out STEMI
Activity restriction: Athletes should avoid competition until symptom-free (expert consensus).

Special Populations

Autoimmune / Connective Tissue Disease

  • SLE: pericarditis usually accompanies disease flare; typically mild; cardiac tamponade rare (1–2%)
  • RA: clinically significant pericarditis in only 1–2%; can progress to constrictive pericarditis over months; predominantly seropositive males
  • Systemic sclerosis: pericardial disease common, especially in diffuse SSc; usually small effusions, rarely hemodynamically significant

Uremic Pericarditis

  • Occurs in ESRD (hemodialysis > peritoneal dialysis); one of the most common causes of cardiac tamponade
  • ECG often normal (unlike typical pericarditis)
  • Treatment: intensive dialysis, indomethacin 25 mg TID; steroids (prednisone 50 mg QD or intra-pericardial) for non-responders
  • Can progress to constrictive pericarditis → pericardial window or pericardiectomy

Pediatric Pericarditis

  • Usually self-limited and benign
  • Common causes: viral, bacterial (~30%; pneumococcus, S. aureus, meningococcus, H. influenzae), ARF, SLE, uremia, post-pericardiotomy syndrome, leukemia/lymphoma, TB

Prognosis & Complications

OutcomeFrequency
Complete recovery within 1 week~60%
Complete recovery within 3 weeks~80%
RecurrenceUp to 30%
Conversion to constrictive pericarditisHigher in nonviral/nonidiopathic forms
Risk factors for recurrence: fever, pericardial effusion, subacute course, failure of initial NSAID therapy.
Ventricular dysrhythmias in pericarditis should prompt suspicion of concurrent myocarditis, a different cardiac disease, or misdiagnosis.

Recent Evidence

A 2026 systematic review (PMID 41276190, Int J Cardiol) reviewed all published cases of drug-induced pericarditis, highlighting this as an under-recognized cause to consider in the diagnostic workup.

Sources: Rosen's Emergency Medicine, 10e | Braunwald's Heart Disease, 12e | Fuster and Hurst's The Heart, 15e | The Washington Manual of Medical Therapeutics
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