**1. Introduction**

Patients with pericardial disease can present to the anaesthesiologist for a variety of diagnostic procedures or therapeutic interventions. Providing safe anaesthesia care for these patients is challenging because of their primary pericardial pathology and significant co-morbidities affecting other organ systems. A thorough understanding of the pathophysiology of the pericardial disease state and its effect on overall haemodynamic variables is necessary before formulating a peri-operative care plan. A multidisciplinary approach involving cardiology, surgical, anaesthesia and critical care teams is needed to provide optimal peri-operative care.

This chapter will examine the basic physical and physiological principles that govern the pathological states of pericarditis, pericardial effusion, tamponade and constrictive pericarditis. A thorough understanding of these principles is required prior to the induction of anaesthesia.

#### **2. Normal anatomy and physiology**

#### **2.1 Normal anatomy**

The normal pericardium is situated in the anterior mediastinum surrounding the heart and proximal portions of the great vessels [1–7]. It is composed of

#### *Inflammatory Heart Diseases*

two layers: an inner visceral layer which is thin, adherent to and continuous with the epicardium of the heart and an outer parietal layer which is thicker and more fibrous. Normal pericardial thickness is 1–2 mm [8]. The parietal and visceral layers are separated by a small amount of serous fluid [1–8]. In non-disease states, approximately 15–50 ml of fluid is contained within the pericardial sac. This fluid is produced by visceral mesothelium cells and is drained from the pericardial space via the lymphatic system to the right side of the heart.

The pericardium is fixed in its anatomical position to the diaphragm and sternum via the pericardio-phrenic and sterno-pericardial ligaments, respectively [4]. Posteriorly, the loosely bound connective tissue anchors it to structures contained within the posterior mediastinum.

Vascular supply is from the pericardio-phrenic artery which is a branch of the internal thoracic artery. Venous drainage is via the pericardio-phrenic veins which drain into the brachiocephalic veins bilaterally. The phrenic nerve provides sensory innervation and the sympathetic trunks' vasomotor innervation [4].

The reflections of the pericardium surrounding the great vessels form two potential spaces called the oblique and transverse sinuses which can be visualised on echocardiographic imaging [4, 8]. The larger oblique sinus forms posteriorly between the left atrium and pulmonary veins. The transverse sinus too lies behind the left atrium, posterior to the aorta and pulmonary trunk [4]. Both sinuses are common sites for blood to collect post-cardiac surgery. Because of the formation of these two sinuses, the left atrium is not entirely an intra-pericardial structure.

#### **2.2 Normal physiology and functions of the pericardium**

Although normal cardiovascular function can occur in the absence of the pericardium, it does bestow certain physiological benefits [1–8]. Because of its relatively fixed ligamentous attachments, the pericardium stabilises the heart in its anatomic position and limits excessive movement within the chest cavity particularly with changes in body position. The pericardial fluid minimises friction exerted on the epicardium from normal heart movements during the cardiac cycle and serves to balance hydrostatic pressures over the surface of the heart. The pressure exerted on the cardiac chambers by the pressure within the intra-pericardial space prevents acute distention of the chambers and helps optimise atrial and ventricular coupling and filling. The pericardial sac serves as a physical barrier against the spread of infection or neoplastic disease within the mediastinum. Prostaglandins secreted by mesothelial and endothelial cells of the pericardium regulate autonomic cardiac reflexes, modulate myocardial contractile function and influence epicardial coronary artery tone.
