The mechanism of death following cardiac tamponade is

Cardiac tamponade kills by compression of the heart from fluid accumulating in the pericardial sac, which restricts cardiac filling during diastole. The pericardium is a relatively inelastic sac, so even a modest rapid increase in pericardial fluid dramatically raises intrapericardial pressure. This elevated pressure equalizes with and then exceeds the pressure inside the cardiac chambers during diastole, preventing the ventricles from filling adequately. The result is severely reduced stroke volume and cardiac output, leading to obstructive shock and ultimately death if untreated. The option describing overdistension of the ventricles due to heart failure is the opposite physiology — in tamponade, the ventricles are compressed and underfilled, not overdistended. Continuous spasm of coronary arteries describes vasospastic angina, an entirely separate condition. Increased cardiac contraction due to inflammation surrounding a myocardial infarction is not the mechanism of tamponade and does not accurately describe how pericardial effusion causes death. The classic clinical triad of tamponade — hypotension, distended neck veins, and muffled heart sounds (Beck's triad) — directly reflects this mechanism of impaired diastolic filling and reduced cardiac output from external compression.