ventricular free wall rupture

Ventricular free wall rupture is rupture of the thin ventricular wall following acute myocardial infarction, allowing blood to escape into the pericardium. It typically occurs 3-7 days post-MI (peak incidence day 3-4) during the inflammatory phase of infarction when the necrotic myocardium is weakest (before collagen deposition has occurred). Risk factors include: transmural (full-thickness) infarction, anterior wall location (higher mortality than inferior), first MI (no prior scar remodeling), delayed reperfusion or failed thrombolysis, and female sex. Presenting signs include sudden cardiovascular collapse, electromechanical dissociation (pulseless electrical activity), Beck's triad (hypotension, elevated JVP, muffled heart sounds) if tamponade develops slowly. Some ruptures are self-limiting if contained by clot and pericardium, creating a pseudoaneurysm or contained rupture (can survive hours/days). Sudden massive rupture causes rapid hemopericardium and tamponade with sudden death. Diagnosis requires high clinical suspicion; echocardiography shows pericardial effusion, right atrial collapse, or visualization of rupture site. Management of contained rupture includes urgent cardiothoracic surgery (primary closure ± patch); supportive measures include fluids for tamponade (preload optimization before pericardiocentesis), though surgical repair is definitive. Mechanical complications of MI include ventricular free wall rupture, ventricular septal defect (VSD), and papillary muscle rupture. Overall mortality of free wall rupture approaches 90%.