**1. Age-related pericardial anatomical changes**

The pericardium is subject to age-related changes just like any other organ in the human body although available literature regarding pericardial anatomy and pericardial disease etiology related to aging is very limited. One study examining bovine pericardium for age-dependent differences in collagen alignment showed higher elasticity, higher tensile strength, and thin pericardium in neonatal compared to adult bovine pericardium [1]. Despite such noted anatomical changes in the pericardial structure with age, the spectrum of pericardial disease remains similar among younger and older populations. Although most guidelines have not discussed specific age-related pericardial disease management, diagnostic evaluation and treatment of pericarditis in the geriatric population should take comorbidities into consideration for optimal management [2].

### **2. Pericardial effusion**

The pericardial space contains 20–50 mL of fluid in the pericardial sac which works as a lubricant between two layers of pericardium. Pericardial effusion is defined by an excess fluid collection over the normal physiological amount within this space. Pericardial fluid accumulation can be secondary to increased fluid

production (i.e., any inflammatory condition) or from reduced fluid reabsorption (i.e., heart failure, pulmonary hypertension, and pericardial lymphatic obstruction). The fluid starts accumulating according to gravitational forces, initially in the posterior-inferior site then circumferentially resulting in moderate to large effusion.

Pericardial effusion can be classified based on various characteristics such as size (mild, moderate, and large), onset (acute, subacute, and chronic), distribution (localized or circumferential), composition (transudate, exudate, blood, or rarely gas from bacterial infections), and hemodynamic effects (without tamponade, with tamponade, effusive-constrictive) [2, 3]. (**Table 1**).

The normal pericardium is made up of a high content of collagen fibers, which creates a relatively inelastic sac that contains the heart. The pressure-volume curve of the normal pericardium is a J-shaped curve, which allows a limited stretch of the pericardium in response to physiological events such as posture or volume status without significant change in the intrapericardial pressure; however, after reaching a certain intrapericardial volume, the intrapericardial pressure rises suddenly and can cause sudden systemic hemodynamic derangements. The rapid rate of the fluid collection also plays a role in the pressure-volume curve; a sudden rise in intrapericardial volume (such as with aortic dissection or trauma with hemopericardium) of 100–200 mL significantly raises the intrapericardial pressure, whereas the slow collection of fluid may allow the development of a large pericardial effusion (1–2 L) without signs of cardiac tamponade [3, 4].
