The pericardium consists of two layers. The inner layer, the visceral pericardium, is a single layer of mesothelial cells that is closely adherent to the myocardium. The outer layer, the parietal pericardium, forms a tough fibrous structure and is composed of dense collagen bundles and a small number of elastic fibers. The two layers are separated by a small amount of pericardial fluid.

The parietal pericardium attaches superiorly to the ascending aorta and the superior vena cava. From there, it continues across the superior vena cava, over the right border of the heart and the pulmonary veins, and encircles the inferior vena cava. After the parietal pericardium crosses the inferior vena cava, the inferior pericardium is densely adherent and essentially one with the diaphragm. The parietal pericardium then turns superiorly, just beyond the apex of the heart, and continues over the pulmonary veins, back to the aorta.

There are two sinuses within the pericardial space. They are formed by the pattern of pericardial reflections around the pulmonary vein and the vena cavae posteriorly. The transverse sinus is posterior to the ascending aorta and the pulmonary artery and is anterior to the atria and the superior vena cava. The oblique sinus is located directly behind the left atrium, centered between the pulmonary veins.

The normal pericardium contains 15 to 50 ml of serous fluid. The pericardial fluid acts as a lubricant that reduces friction between the pericardial membranes during each heartbeat. Owing to the tough fibrous structure of the parietal pericardium, the pericardial sac is relatively noncompliant. As a result, alterations in the pericardium can have an impact on cardiac hemodynamics.

There are several disease processes that can cause pericardial effusions (Table 28.1). Secondary malignancies (usually from the lung or the breast) are the most common causes of pericardial effusions.

A wide variety of therapeutic options are available to manage pericardial effusions. These options include simple observation,
use of anti-inflammatory or antineoplastic chemotherapy, pericardiocentesis, percutaneous balloon pericardiotomy, and surgery. Because of the lack of prospective studies evaluating the efficacy of the different treatments, the optimal management of this condition remains a matter of controversy.

When determining the choice of treatment for pericardial effusions, a number of factors need to be considered. These factors include the presence or absence of tamponade, the underlying diagnosis or etiology of the effusion, the potential for recurrence, and the resources available at one’s institution.

Percutaneous balloon pericardiotomy is performed in the cardiac catheterization laboratory using local anesthesia and intravenous sedation, with fluoroscopic and echocardiographic guidance. The pericardium is entered with an 18-gauge pericardial needle by use of a standard subxiphoid approach. A guide wire is then advanced into the pericardial space, a catheter is introduced, and pericardial fluid is drained for laboratory studies. Radiographic contrast medium is then injected into the pericardial space to aid visualization. The catheter is removed, and the tract is dilated using a 10F-14F dilator. A lowprofile balloon-dilating catheter containing some radiographic contrast medium is inserted over the guide wire and positioned across the parietal pericardium. To ensure adequate opening of the parietal pericardium, a series of balloon inflations are performed. A pigtail catheter is often left in the pericardial space for 24 hours and removed once complete resolution of the effusion has been confirmed by echocardiography. Chest X-rays are also performed after the procedure to exclude the possibility of a pneumothorax.

There have been several small studies describing the use of this modality as an alternative to a surgically created pericardial window. The largest trial, which was part of a multicenter registry, involved 50 patients. In that trial, the modality was considered successful for 46 patients, after a mean follow-up of 3.6 months. The procedure was deemed unsuccessful for four patients, either because of recurrence of effusion or tamponade, bleeding requiring surgical intervention, or persistent catheter drainage requiring surgery.

Subxiphoid pericardial window is a surgical procedure that can be performed with the patient under either local or general anesthesia. Because of the lack of evidence in the literature, the optimal anesthetic management for patients with pericardial tamponade who require a subxiphoid pericardial window remains open to debate. The advantages of using general anesthesia include improved surgical evacuation of pericardial contents and improved patient comfort. In cases where general anesthesia is administered to patients with significant hemodynamic compromise, the patient should be prepped and draped, with the surgeon ready to begin, before induction of general anesthesia. Unpublished data have also suggested that there is no difference in outcomes between patients managed with local anesthesia and sedation and those managed with general anesthesia (Fig. 28.1).