Harvey's Garden

Acute pericarditis

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Etiology

  • Idiopathic
  • Infectious
    • Most commonly viral (e.g., coxsackie B virus)
    • Bacterial (e.g., Staphylococcus spp., Streptococcus spp.)
    • TB: Rare in the US/developed nations, but the most common cause of pericarditis in developing nations and endemic areas. c
  • Myocardial infarction
    • Postinfarction fibrinous pericarditis: within 1–3 days as an immediate reaction
    • Dressler syndrome: weeks to months after an acute myocardial infarction
  • Postoperative (postpericardiotomy syndrome): due to blunt or sharp trauma to the pericardium
  • Uremia: e.g., due to acute or chronic renal failure
    • Accumulated toxins promote inflammation.
  • Radiation
  • Neoplasms (e.g., Hodgkin lymphoma)
  • Autoimmune connective tissue diseases (e.g., rheumatoid arthritis, SLE, scleroderma)
  • Trauma

Classifications

  • Serous Pericarditis
  • Fibrous or Fibrinous Pericarditis
    • Most common pericarditis
    • MI (Dressler syndrome)
    • Rheumatic fever
    • Uremia
    • TB pericarditis
    • Malignancy involvement
    • Pericardial surface covered by shaggy, fibrinous exudate
    • “Bread and Butter” appearance
  • Purulent (Suppurative) Pericarditis
    • Pyogenic bacteria (Staphylococci, Streptococci, Pneumococci)
    • Direct extension / hematogenous or lymphatic spread / direct implant
    • Severe acute infection
    • Pericardial surface covered by purulent exudate and infiltrated by neutrophils
  • Hemorrhagic Pericarditis
    • Malignancy involvement
    • TB pericarditis
    • Severe acute infection
    • Admixture of inflammatory effusion with blood

Clinical features

Acute pericarditis

  • Chest Pain (CP): Pleuritic, sharp, retrosternal.
  • Positional: Worse when supine; relieved by leaning forward.
  • Radiation: Trapezius ridges (pathognomonic; phrenic nerve irritation).
  • Physical Exam (PE): Pericardial Friction Rub (high-pitched, scratching/velcro sound; heard best at LLSB with pt leaning forward during expiration).

Chronic pericarditis

Constrictive pericarditis

  • Pathophysiology: A late complication (sequela). Chronic fibrosis, scarring, and calcification of the pericardium leading to a rigid, non-compliant sac.
  • Symptoms of fluid overload (i.e., backward failure)

Hepatojugular Reflux (HJR) and Jugular vein distention (JVD)

  • Kussmaul Sign: Paradoxical rise in JVD with inspiration (impaired RV filling). c
  • Pericardial Knock: High-frequency early diastolic sound (caused by sudden cessation of ventricular filling). c
    • Differ from S3, which is low-frequency early diastolic sound

Diagnostics

Acute pericarditis

  • Clinical Dx: Requires ≥2 of 4: (1) Characteristic CP, (2) Friction rub, (3) EKG changes, (4) New/worsening pericardial effusion.
  • Initial/Screening (EKG):
    • Diffuse ST-elevation (concave/up-sloping) and PR-segment depression (highly specific). c
    • Note: aVR will show ST-depression and PR-elevation.
  • Key Labs: ↑ ESR, ↑ CRP, mild leukocytosis. ↑ Troponin I/T suggests perimyocarditis.
  • Imaging:
    • CXR: Usually normal. “Water-bottle heart” if large effusion (>200mL) present.
    • Echocardiogram: Initial test to rule out effusion or tamponade; often normal in uncomplicated pericarditis.

Chronic pericarditis

  • Imaging
    • CT and cardiac MRI
      • Pericardial thickening > 2 mm
      • Calcifications

Treatment

  • First-line (Idiopathic/Viral): NSAIDs (Ibuprofen or Indomethacin) + Colchicine (colchicine significantly ↓ recurrence rate). c
  • Second-line / Refractory: Corticosteroids (Prednisone). Note: Avoid steroids as first-line unless NSAIDs are contraindicated (e.g., pregnancy, severe renal disease) or if etiology is autoimmune, due to high risk of recurrence.
  • Etiology-Specific Variants:
    • Post-MI: Aspirin + Colchicine (Avoid other NSAIDs & steroids; they impair myocardial scar formation and ↑ risk of ventricular free wall rupture).
    • Uremic Pericarditis: Hemodialysis (NSAIDs/colchicine are ineffective and contraindicated).

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