Explanation

Pathophysiology  Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which, in turn, can evoke a pericardial effusion.  This often leads to pericardial organization, chronic fibrotic scarring, and calcification, most often involving the parietal pericardium  In constrictive pericarditis, the easily distensible, thin parietal and visceral pericardial linings become inflamed, thickened, and fused.  Because of these changes, the potential space between the linings is obliterated, and the ventricle loses distensibility.  Venous return to the heart becomes limited, and ventricular filling is reduced, with associated inability to maintain adequate preload.  Filling pressures of the heart tend to become equal in both the ventricles and the atria.  Since the myocardium is unaffected, early ventricular filling during the first third of diastole is unimpeded