Pericarditis

Pericarditis – High-Yield Study Guide for Medical Students

Definition

Pericarditis is inflammation of the pericardial sac, which may present as an isolated acute episode, recur as relapsing pericarditis, or evolve into chronic constrictive disease with impaired ventricular filling. It ranges from mild, self-limited viral disease to life-threatening purulent or effusive-constrictive forms. Relapsing pericarditis is defined as at least two episodes of acute pericarditis separated by a symptom-free interval of at least 4–6 weeks.^[1][2]

Epidemiology

Pericarditis is one of the most common causes of acute chest pain in young adults presenting to the emergency setting after myocardial ischemia and pulmonary embolism. Most cases in high-income countries are presumed viral or idiopathic, whereas tuberculous and purulent forms remain more prevalent in low-resource settings. Autoimmune disease–related pericarditis (e.g., in systemic lupus erythematosus and rheumatoid arthritis) and post–cardiac injury syndromes are increasingly recognized due to greater use of cardiac surgery, percutaneous interventions, and advanced imaging.^[3][4]

Relapsing pericarditis affects a subset of patients after an initial acute episode; risk factors include inadequate initial anti-inflammatory therapy, early steroid use, and underlying autoimmune disorders.^[2]

Etiology and Classification

Pericarditis can be classified by time course, etiology, and hemodynamic impact.

• By time course
  • Acute: <4–6 weeks.
  • Incessant: >4–6 weeks but <3 months without remission.
  • Recurrent (relapsing): new episode after ≥4–6 weeks symptom-free interval.
  • Chronic: >3 months, often with constrictive physiology.
• By etiology
  • Idiopathic/viral: most common in developed countries.
  • Bacterial: including purulent pericarditis (e.g., Staphylococcus, Streptococcus), tuberculosis.
  • Autoimmune/inflammatory: SLE, RA, systemic sclerosis, autoinflammatory syndromes.
  • Post–cardiac injury: post-pericardiotomy syndrome, post-MI (Dressler), post-ablation, post-trauma.^[4]
  • Metabolic: uremic pericarditis, hypothyroidism.
  • Neoplastic: direct invasion or metastatic spread (lung, breast, lymphoma).
  • Radiation-induced.
  • Drug-induced: e.g., hydralazine, isoniazid, some immune checkpoint inhibitors (via autoimmune mechanisms).
• By hemodynamics
  • Simple inflammatory without major hemodynamic effect.
  • Pericarditis with effusion.
  • Cardiac tamponade.
  • Constrictive pericarditis (chronic fibrotic, often calcific pericardium).
  • Effusive-constrictive pericarditis with both effusion and constrictive physiology.^[5]

Pathophysiology

The pericardium is a double-layered sac (visceral and parietal layers) with a thin film of lubricating fluid that stabilizes the heart and limits acute chamber dilation. In pericarditis, an inciting insult triggers an inflammatory cascade with vasodilation, increased vascular permeability, and leukocyte recruitment in the pericardial layers.

In acute disease, this leads to fibrin deposition and exudative fluid accumulation, generating the classical fibrinous “friction rub” and pleuritic chest pain as inflamed layers rub against each other. Persistent or severe inflammation can result in:

• Pericardial effusion: fluid accumulation may be serous, serofibrinous, hemorrhagic, or purulent.
• Cardiac tamponade: rapid or large effusion raises pericardial pressure, impairs diastolic filling, and reduces stroke volume.
• Chronic constriction: repeated inflammation and healing cause pericardial thickening, fibrosis, and sometimes calcification, creating a rigid shell that limits diastolic expansion and generates equalization of diastolic pressures in all chambers.^[6][7]

Effusive-constrictive pericarditis combines a tense effusion with an intrinsically noncompliant pericardium; pericardiocentesis may not fully normalize intracardiac pressures because constriction persists.^[5]

Clinical Presentation

Symptoms

• Chest pain: classically sharp, pleuritic, retrosternal or left precordial, often radiating to the trapezius ridge or shoulders.
• Positional component: worse in supine position, improved by sitting up and leaning forward.
• Dyspnea: particularly with exertion or in tamponade/large effusion.
• Low-grade fever: more common in infectious or autoimmune etiologies.
• Viral prodrome: myalgias, malaise, upper respiratory symptoms in idiopathic/viral cases.
• Palpitations: due to sympathetic activation or associated arrhythmias.

Physical Examination

• Pericardial friction rub: a high-pitched, superficial, scratchy sound best heard at the left sternal border with the patient leaning forward, often triphasic (atrial systole, ventricular systole, early diastole). It is highly specific but transient.
• Tachycardia and sometimes low-grade fever.
• Signs of pericardial effusion/tamponade (if present):
  • Elevated JVP.
  • Tachycardia and hypotension in advanced tamponade.
  • Muffled heart sounds and pulsus paradoxus.
• Signs of constriction in chronic disease:
  • Elevated JVP with prominent y descent.
  • Kussmaul sign (jugular venous distension that increases on inspiration).
  • Pericardial knock (early diastolic sound).
  • Peripheral edema, ascites, hepatomegaly mimicking right-sided heart failure.

Diagnostic Criteria for Acute Pericarditis

Acute pericarditis is diagnosed clinically when at least two of four classic criteria are present:^[1]

• Characteristic chest pain.
• Pericardial friction rub.
• Typical ECG changes (widespread ST elevation and/or PR-segment depression).
• New or worsening pericardial effusion.

Supportive findings include elevated inflammatory markers (CRP, ESR, leukocytosis) and pericardial inflammation on imaging (e.g., cardiac MRI).

Electrocardiography

The ECG classically evolves through four stages, though not all are seen in every patient:

• Stage I: diffuse concave-upward ST-segment elevation and PR depression (except aVR and often V1, which show reciprocal ST depression and PR elevation).
• Stage II: normalization of ST segments; T waves may flatten.
• Stage III: T-wave inversion after ST segments normalize.
• Stage IV: normalization of ECG over days to weeks.

Unlike MI, ST elevation in pericarditis is diffuse, not localized to a single coronary territory, and there are usually no Q waves or reciprocal ST depression (except aVR/V1). Low-voltage QRS and electrical alternans raise concern for large effusion and tamponade.

Laboratory Evaluation

• Inflammatory markers: CRP and ESR are typically elevated; serial CRP can help guide therapy duration and risk of relapse.^[2]
• Cardiac biomarkers: mild troponin elevation suggests concomitant myocardial involvement (myopericarditis) but usually with preserved LV function.
• Etiologic workup as indicated by context: CBC, renal function, thyroid panel, blood cultures (if febrile), autoimmune panel (ANA, RF, etc.), TB testing, HIV, and malignancy evaluation when appropriate.

Imaging

Transthoracic Echocardiography (TTE)

TTE is the first-line imaging modality in suspected pericarditis. It assesses for pericardial effusion, hemodynamic compromise, and features of constriction.^[6]

• Findings in acute pericarditis:
  • Pericardial effusion (if present): anechoic or complex space between pericardial layers.
  • Normal or mildly reduced LV systolic function in isolated pericarditis.
• Findings in tamponade:
  • Right atrial and right ventricular diastolic collapse.
  • Exaggerated respiratory variation in transvalvular Doppler inflow (mitral and tricuspid).
  • Dilated IVC with reduced inspiratory collapse.
• Findings in constrictive pericarditis:
  • Septal bounce and interventricular dependence.
  • Respiratory variation in mitral and tricuspid inflow velocities (ventricular interdependence).
  • Hepatic vein flow reversal and abnormal tissue Doppler (medial e′ relatively preserved vs lateral).

Cardiac CT and Cardiac MRI

Cardiac MRI (CMR) and CT provide detailed assessment of pericardial thickness, inflammation, and calcification and are especially useful when echocardiography is non-diagnostic or constriction is suspected.^[6]

• Cardiac MRI:
  • Can show pericardial thickening and edema on T2-weighted images.
  • Late gadolinium enhancement (LGE) highlights active pericardial inflammation.
  • Real-time cine imaging during respiration demonstrates ventricular interdependence and septal shift in constriction.
• Cardiac CT:
  • Excellent for visualization of pericardial calcification and thickness.
  • Helps differentiate constrictive pericarditis from restrictive cardiomyopathy.

Pericardiocentesis and Pericardial Biopsy

Pericardiocentesis is primarily indicated for hemodynamically significant effusion or tamponade and for diagnostic evaluation in suspected bacterial, tuberculous, malignant, or uremic pericarditis. Fluid analysis includes cell count, Gram stain and culture, cytology, protein and LDH, and targeted tests (e.g., ADA for TB). Pericardial biopsy or pericardiectomy specimens may be needed for definitive diagnosis in chronic, unexplained, or recurrent cases.^[1]

Management of Acute Pericarditis

Management aims to control inflammation, relieve pain, treat underlying causes, and prevent complications or recurrences. Risk stratification is essential to decide on outpatient versus inpatient care and the intensity of etiologic workup.

General Principles

• Identify high-risk features (e.g., high fever, subacute course, large effusion, tamponade, failure to respond to NSAIDs, elevated troponin, immunosuppression, trauma, or anticoagulation) which necessitate more intensive evaluation and closer monitoring.
• Exercise restriction during active inflammation and for several weeks after symptom resolution to reduce risk of relapse and arrhythmia, particularly in athletes.^[2]

Pharmacologic Therapy

• NSAIDs (first-line):
  • Agents: ibuprofen, high-dose aspirin, or indomethacin.
  • Typical duration: 1–2 weeks at full dose, then taper guided by symptoms and CRP.
• Colchicine (key adjunct):
  • Add-on to NSAIDs significantly reduces symptom duration and risk of recurrence in both acute and recurrent pericarditis.
  • Usually continued for 3 months in first episodes and 6 months or more in recurrent cases, with dose adjustment for renal impairment and weight.
• Glucocorticoids:
  • Reserved for specific indications such as autoimmune disease, uremic pericarditis unresponsive to dialysis, or NSAID/colchicine intolerance or contraindications.
  • Use the lowest effective dose with slow taper; early or high-dose steroids increase recurrence risk in idiopathic cases.^[1][2]

Management of Recurrent (Relapsing) Pericarditis

Recurrent pericarditis is challenging and requires strategies to reduce flare frequency and steroid dependence.

• Optimize NSAID and colchicine therapy, often with longer treatment and slower taper guided by CRP.
• Avoid or minimize glucocorticoids when possible; if needed, use low-to-moderate doses with very gradual taper.
• Consider targeted immunomodulation in steroid-dependent or colchicine-resistant cases, such as IL-1 blockers (e.g., anakinra, rilonacept) in specialized settings, based on emerging evidence.^[2]
• Investigate secondary causes thoroughly, including autoimmune disease, autoinflammatory syndromes, and neoplasia.

Management of Pericardial Effusion and Tamponade

• Hemodynamically stable effusions can be managed with anti-inflammatory therapy and close follow-up, with serial echocardiography to assess size and impact.
• Cardiac tamponade requires urgent pericardiocentesis or surgical drainage plus treatment of the underlying cause.
• Effusive-constrictive pericarditis may need both pericardiocentesis and eventually pericardiectomy if constriction persists after effusion removal.^[5]

Management of Constrictive Pericarditis

Constrictive pericarditis leads to chronic right-sided heart failure symptoms and requires careful differentiation from restrictive cardiomyopathy.

• Medical therapy (diuretics, sodium restriction) can temporarily relieve congestion but does not correct the mechanical constraint.
• Surgical pericardiectomy is the definitive treatment for chronic symptomatic constriction, particularly in patients with functional limitation and acceptable operative risk. Advanced imaging (CT, MRI) and hemodynamic catheterization help confirm diagnosis and plan surgery.^[7]
• Outcomes depend on etiology (e.g., worse in radiation-induced disease) and comorbidities.

Pericarditis in Autoimmune Disease

Pericarditis is a recognized cardiac manifestation of systemic autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, and systemic sclerosis. These patients may present with acute, recurrent, or chronic pericardial involvement, sometimes with effusion or tamponade.^[3][8]

• Management often requires coordination between cardiology and rheumatology.
• Immunosuppressive therapy (e.g., steroids, DMARDs, biologics) is tailored to the underlying systemic disease and severity of pericardial involvement.
• Advanced imaging (CMR, CT) is often helpful in characterizing pericardial inflammation versus other cardiac complications (e.g., myocarditis, pulmonary hypertension).

Prognosis and Complications

Most idiopathic or viral acute pericarditis cases are self-limited with appropriate treatment, but a subset progress to recurrent disease or chronic complications.

• Early complications:
  • Large effusion and cardiac tamponade.
  • Myopericarditis (myocardial involvement) with transient LV dysfunction.
  • Purulent pericarditis with high mortality if not promptly treated.
• Late complications:
  • Recurrent pericarditis with multiple flares over months or years.
  • Chronic constrictive pericarditis.
  • Effusive-constrictive pericarditis.

Risk of progression to constriction is higher in specific etiologies such as tuberculous, purulent, post-radiation, and autoimmune pericarditis.^[1]

Key Clinical Pearls for Exams and Practice

• Pleuritic chest pain that improves when sitting up and leaning forward is highly suggestive of pericarditis; always think of this in young patients with chest pain and non-ischemic ECG changes.
• Pericardial friction rub is highly specific but can be transient; auscultate multiple times and in different positions.
• ECG hallmark: diffuse concave ST elevation with PR depression; absence of reciprocal ST depression (except aVR/V1) distinguishes it from STEMI.
• Echocardiography is mandatory in suspected pericarditis to evaluate for effusion and tamponade and should be repeated if clinical status worsens.^[6]
• Colchicine + NSAID is the evidence-based cornerstone of therapy for both acute and recurrent pericarditis; colchicine reduces recurrence risk and is a favorite exam point.^[2]
• Use glucocorticoids cautiously in idiopathic pericarditis, as they are associated with higher recurrence rates; reserve them for clear indications such as autoimmune disease or NSAID/colchicine contraindication.^[1]
• Recurrent pericarditis should prompt a search for underlying autoimmune or autoinflammatory disease, and management may require prolonged colchicine and immunomodulatory therapy.
• Constrictive pericarditis can mimic right-sided heart failure or cirrhosis; look for Kussmaul sign, pericardial knock, and imaging evidence of pericardial thickening and septal bounce. Surgical pericardiectomy is the definitive therapy.^[7]
• Effusive-constrictive pericarditis is suggested when tamponade hemodynamics persist despite adequate pericardial fluid drainage, due to intrinsic pericardial constriction.^[5]
• In systemic autoimmune diseases such as SLE, pericarditis may signal increased systemic activity and should prompt comprehensive evaluation of other organ systems.^[3][8]

Summary

Pericarditis is a common and clinically important cause of chest pain and hemodynamic compromise. A solid understanding of its pathophysiology, clinical presentation, and diagnostic approach allows timely differentiation from life-threatening mimics like acute coronary syndrome and pulmonary embolism. Evidence-based management focuses on NSAIDs and colchicine, careful risk stratification, and targeted use of advanced imaging and invasive procedures. Recognizing high-risk etiologies and complications such as tamponade and constrictive pericarditis is essential for both examinations and real-world practice.