Cardiac tamponade pathophysiology

Pathophysiology
The outer pericardium is made of fibrous tissue which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase.

Ordinarily drainage from the pericardium occurs via the thoracic duct and the right lymphatic duct into the right pleural space. In the absence of disease, the normal pericardium contains only 20-50 cc of serous fluid due to ultrafiltration from the blood. Up to about 75 cc can accumulate acutely in the pericardium without hemodynamic compromise. Much greater amounts of fluid can accumulate chronically over a prolonged period of time as the pericardial sac stretches slowly to accommodate the fluid without hemodynamic compromise. However, if the volume of the fluid accumulation is too rapid and or large, then hemodynamic compromise can occur with a rise in pericardial pressure. This in turn reduces stroke volume and eventually cardiac output.

If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to decreased stroke volume. This causes obstructive shock to develop, and if left untreated then Cardiac arrest may occur (in which case the presenting rhythm is likely to be Pulseless electrical activity)

Below is a video demonstrating hemorrhagic effusion leading to cardiac tamponade. 