Constrictive Pericarditis

Constrictive pericarditis develops when inflammation leaves the pericardium thickened, fibrotic and sometimes calcified. The resulting rigid shell cannot expand normally during diastole, so the ventricles compete for a limited intrapericardial volume. Ventricular systolic function is often preserved, but filling is restricted and stroke volume becomes relatively fixed. Cardiac output then depends heavily on adequate venous return and heart rate. The haemodynamic consequence is predominantly systemic venous congestion: raised jugular venous pressure, peripheral oedema, ascites, hepatomegaly, abdominal discomfort, fatigue and exertional breathlessness. Pulmonary oedema is less characteristic than in left-sided systolic failure, although pulmonary venous pressure can rise when filling becomes severely impaired. Causes include previous viral or idiopathic pericarditis, bacterial or tuberculous infection, cardiac surgery, chest radiation, malignancy and immune-mediated disease. The likelihood of progression varies substantially. It is below 1% after viral or idiopathic pericarditis, approximately 2–5% with immune-mediated or neoplastic pericarditis, and approximately 20–30% after bacterial disease, particularly purulent or tuberculous infection. Chronic constriction only rarely follows an uncomplicated episode of idiopathic acute pericarditis.