The pericardium surrounds the heart and the great blood vessels and is composed of a thin visceral membrane, a fibrous parietal membrane, and the pericardial space between the membranes, which normally contains less than 50 mL of pericardial fluid (Braunwald [24], Petrofsky [229]). Understanding the properties of the pericardium can help to predict changes within the heart under physiological stress. The pericardium plays a pivotal role in the distribution forces across the heart, playing a significant role in the physiological concept of ventricular interdependence whereby changes in pressure, volume and function in one ventricle influence the function of the other (Little and Freeman [148], Strimel [278]).

The parietal membrane is composed primarily of collagen and elastin fibres, which give the membrane some elasticity (Braunwald [24]). As a result of this elasticity, the normal pericardium has a non‐linear pressure–volume curve.

In non‐altered function the right atrium and ventricle fill during inspiration; the pericardium limits the ability of the left‐sided chambers to dilate. This contributes to the bowing of the atrial and ventricular septa to the left, which reduces left ventricular filling volumes and leads to a drop in cardiac output. Intrapericardial pressures rise, as occurs in the development of a pericardial effusion. Small pericardial fluid volume changes do not generally result in any change in pericardial pressure, but a large sudden increase in pericardial volume can cause a steep change in pericardial pressure, which can lead to a clinically significant fall in stroke volume leading to tamponade (Imazio and Adler [116]). With a slowly enlarging pericardial effusion, the pericardial membranes stretch to accommodate the growing fluid volume without any significant change in the pericardial pressure until the limit of pericardial membrane stretch is reached (Little and Freeman [148], Strimel [278]).