Pericarditis, Constrictive

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

Diagnosis

• 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

Treatment

• 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