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For further information, see CMDT Part 10-52: Constrictive Pericarditis

Key Features

  • Generally caused by inflammation leading to a thickened, fibrotic, adherent pericardium that restricts diastolic filling and produces chronically elevated venous pressures

  • Causes

    • Cardiac surgery

    • Radiation therapy

    • Connective tissue disorders

  • Some cases secondary to

    • Trauma

    • Drugs

    • Asbestosis

    • Sarcoidosis

    • Uremia

  • May coexist with pericardial tamponade, a condition also referred to as effusive-constrictive pericarditis

Clinical Findings

  • Slowly progressive dyspnea, fatigue, and weakness

  • Chronic edema, hepatic congestion, and ascites out of proportion to degree of peripheral edema

  • Elevated jugular venous pressure with a rapid y descent

  • Failure of jugular venous pressure to fall during inspiration (Kussmaul sign)

  • Pericardial knock in early diastole

  • Atrial fibrillation is common

  • Pulsus paradoxus is unusual


  • Chest radiograph

    • Normal heart size or cardiomegaly

    • Pericardial calcification is rare since TB is cause less often; best seen on lateral view

  • Echocardiography

    • Rarely demonstrates thickened pericardium

    • Septal bounce, respiratory fall in mitral Doppler filling pattern useful

  • CT and MRI may be more sensitive than echocardiography, but can only identify a thickened pericardium when it is > 4 mm

  • Cardiac catheterization: Right atrium (RA)

    • Elevated pressure with y descent > x descent

    • Kussmaul sign (lack of fall of RA pressure with inspiration)

    • "Square root" diastolic pressures in both RV and LV

    • Equalization of diastolic pressures

    • RV end-diastolic pressure > one-third of RV systolic pressure

    • Evidence of RV-LV interaction (discordance in RV/LV systolic pressures with inspiration)

    • Area of RV/LV pressure tracing ratio that decreases with inspiration

  • The only definitive way to diagnose effusive-constrictive pericarditis is to reveal the underlying constrictive physiology once the pericardial fluid is drained


  • Should be aimed at the specific etiology initially

  • Anti-inflammatory medications may have a role if there is evidence of ongoing inflammation

  • Diuretics

    • Mainstay of treatment once hemodynamics are determined

    • Should be aggressive, using loop diuretics (oral torsemide or bumetanide if bowel edema is suspected), thiazides, and aldosterone antagonists (especially in the presence of ascites and hepatic congestion)

  • Pericardiectomy

    • Should be recommended when diuretics are unable to control symptoms

    • Removes only the pericardium between the phrenic nerve pathways

    • However, most patients still require diuretics after the procedure, although symptoms are usually dramatically improved

    • Morbidity and mortality are high (up to 15%) and are greatest in those with the most disability prior to the procedure

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