Inflammation of the pericardium — pleuritic chest pain improved by leaning forward, friction rub, diffuse ST elevation with PR depression.
Also known as: acute pericarditis, pericarditis, viral pericarditis
Overview
Inflammation of the pericardial sac with or without pericardial effusion, defined by at least 2 of: characteristic chest pain, pericardial friction rub, new widespread ST elevation or PR depression on ECG, or new/worsening pericardial effusion.
Epidemiology
Accounts for ~5% of ED chest pain visits with non-ischemic etiology. Most often idiopathic or viral; men 20-50 years most commonly affected.
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Tuberculosis (most common cause worldwide in endemic regions)
Radiation therapy, certain drugs (hydralazine, procainamide, isoniazid)
Pathophysiology
Inflammation of the visceral and parietal pericardium produces increased capillary permeability, fibrin deposition, and exudate. The roughened layers generate friction rub. Sympathetic involvement of the diaphragm (phrenic nerve) causes referred shoulder/trapezius pain. Inflammation may extend to the epicardium (myopericarditis) or produce significant effusion.
Clinical presentation
Symptoms
Sharp, pleuritic, retrosternal or left precordial chest pain
Worse supine, better leaning forward
Radiation to trapezius ridge (highly specific — phrenic nerve)
Low-grade fever, dyspnea, fatigue
Antecedent viral prodrome (URI, GI symptoms) common
Signs / physical exam
Pericardial friction rub — three-component, scratchy, best at LLSB with patient leaning forward
Tachycardia
Low-grade fever
Signs of effusion (muffled heart sounds, Beck triad) if progressing to tamponade
Differential diagnosis
Acute coronary syndrome / STEMI — Regional (not diffuse) ST elevation with reciprocal changes; high troponin; risk factor profile
Pulmonary embolism — Pleuritic pain with dyspnea and hypoxia; S1Q3T3, right heart strain; D-dimer / CTPA
CBC, CRP, ESR (elevated CRP supports diagnosis and guides response to therapy)
BMP, BUN/Cr (uremic etiology)
ANA, RF, TSH if autoimmune cause suspected; HIV and TB testing in appropriate populations
Blood cultures if febrile and effusion present
Imaging
12-lead ECG — diffuse concave ST elevation with PR segment depression (PR elevation in aVR is reciprocal — early sign)
Echocardiography — assess for pericardial effusion and ventricular function (rule out tamponade and myocarditis)
CXR — typically normal; cardiomegaly only with large effusion
Cardiac MRI — late gadolinium enhancement of pericardium; useful for myopericarditis or recurrent disease
Chest CT for suspected purulent or constrictive disease
Diagnostic algorithm
Feature
Pericarditis
STEMI
Early repolarization
ST elevation distribution
Diffuse, concave
Regional, convex
Often precordial
PR depression
Present (PR elevation in aVR)
Absent
Absent
Reciprocal ST depression
Absent (except aVR, V1)
Present
Absent
Q waves
Absent
May develop
Absent
Troponin
Normal or mildly elevated
Markedly elevated
Normal
Evolution
Diffuse ST resolves over days then T inversion
ST resolves, Q waves and T inversion form
Stable over time
ECG and biomarker comparison: pericarditis vs STEMI vs benign early repolarization.
Treatment
First-line
NSAIDs — ibuprofen 600-800 mg PO TID × 1-2 weeks then taper, OR aspirin 750-1000 mg PO TID (preferred post-MI pericarditis)
Colchicine 0.5 mg PO BID (0.5 mg daily if <70 kg) × 3 months — added to NSAID for FIRST episode reduces recurrence (COPE / ICAP trials)
Proton pump inhibitor while on high-dose NSAIDs
Activity restriction until symptoms resolve and CRP normalizes (≥3 months for athletes with myopericarditis)
Treat underlying cause: dialysis for uremia, antimicrobials for purulent, TB therapy if confirmed
Second-line / adjunct
Corticosteroids (prednisone 0.25-0.5 mg/kg/day with slow taper) — reserved for NSAID/colchicine failure, contraindication, or specific etiologies (autoimmune, uremic) — increases recurrence risk in idiopathic disease
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