Pericardial Syndromes

Abstract

Different aetiological agents either infectious or non-infectious (see chapter on the aetiology of pericardial diseases) interact with the pericardium in a rather non-specific way causing inflammation of the pericardium (pericarditis) with possible increased production of pericardial fluid or in some cases reduced reabsorption (pericardial effusion) [1–3]. The pericardium is rather rigid, and sudden changes of its volume may occur only with sudden increase of intrapericardial pressure generating a compressing effect on cardiac chambers and impairing diastolic filling during the entire diastole, thus causing a reduced cardiac output (cardiac tamponade) [3]. On the contrary, slowly accumulating pericardial fluid may occur without the development of cardiac tamponade in other cases (isolate chronic large pericardial effusion) [3]. The final stage of any pathological process affecting the pericardium is represented by fibrosis with possible thickening and calcification leading to a loss of pericardial elasticity and a constrictive effect of the pericardium on cardiac chambers, thus impairing diastolic filling in mid-late diastole (constrictive pericarditis).