Primary Causes & Pathophysiology
Most cases start with viral trigger (germ insult) or immune activation (defence response). Inflamed pericardium (sac lining) releases mediators (chemical signals) causing pain and fibrin (sticky protein) deposit. Fluid may gather as exudate (leaky inflammatory fluid) forming effusion. Large or rapid effusion raises sac pressure causing tamponade (heart compression). Healing may scar and stiffen the sac causing constriction.
Direct viral injury plus immune response inflames the sac
Autoimmune reaction to heart necrosis (tissue death) attacks pericardium weeks later
Retained toxins plus inflammation irritate the pericardium
Immune complexes deposit in pericardium and trigger inflammation
Granulomatous (lumpy immune) bacterial spread causes chronic sac inflammation
Tumour spread directly invades the pericardium
Blood spread or nearby pneumonia seeds pus-forming germs in the sac
Trauma plus immune activation inflames the sac after intervention