The pericardium is a fibroelastic sac that contains the heart and the proximal segments of the aorta and pulmonary artery and a portion of the pulmonary veins and the venae cavae that are close to the heart. Embryologically, the heart invaginates into a spherical area that results in two layers, a visceral layer that is adherent to the heart and a parietal layer that surrounds the heart. The pericardium has two major sinuses that are created by pericardial reflections, the transverse sinus and the oblique sinus. The transverse sinus lies anterior to the superior vena cava and posterior to the aorta and pulmonary trunk. One can place a finger in the transverse sinus by starting at the left atrial appendage area and moving posterior to the great vessels. The transverse sinus continues posteriorly until it comes anteriorly between the superior vena cava and the ascending aorta. The oblique pericardial sinus lies posterior to the heart and can be visualized by lifting the heart and exploring the space between the pulmonary veins. The boundaries of the oblique pericardial sinus on the right are the inferior vena cava and the right pulmonary veins and on the left by the left pulmonary veins. Cardiac surgeons expose these sinuses as they lift the heart to inspect the posterior wall of the heart. The pericardial reflection onto the pulmonary veins limits the degree to
which apex of the heart can be elevated. This anatomic feature becomes important during coronary bypass operations when bypass to posterior coronary vessels is needed. The transverse sinus will allow fluid to accumulate adjacent to the aorta and the pulmonary artery and surround the left atrial appendage. This can cause confusion on echocardiogram when a small amount of pericardial fluid lies adjacent to the ascending aorta. It gives the appearance of a double line that can raise the question of aortic dissection. Fluid in the transverse sinus that surrounds the left atrial appendage exposes the tip of the appendage and in “en face” views gives the appearance of a small mobile mass.

The intrapericardial portions of the above-mentioned vascular structures can become problematic. For example, in the setting of type A aortic dissection, the ascending aorta can “weep” serous fluid or even bleed into the pericardium if the aorta is disrupted. It is noteworthy that the pulmonary veins and a portion of the left atrium are extrapericardial and are not subjected to intrapericardial pressure. In the presence of tamponade or constriction, the extrapericardial relationship between the pleural space and the pericardial space results in only minor changes of flow into the left atrium during inspiration.¹

The pericardial space contains a small amount of fluid, <50 mL, which acts as a lubricant minimizing friction during systole or diastole. This plasmalike, low-protein ultrafiltrate is likely expressed from the visceral pericardium and is drained by the adjacent lymphatic channels. When inflammation is present between the two layers of the pericardium, one can hear a “friction rub” during the systolic, diastolic, and atrial contraction phases of the cardiac cycle.²

These findings will be illustrated in Section 2: Pericardial Effusion.

The fibroelastic pericardial sac has elastic limits and can cause difficulty when pericardial fluid accumulates. Increased pericardial pressure is manifest by collapse of chambers that have the lowest pressure such as the right atrium and right ventricle. This collapse occurs during the phase of the cardiac cycle when the chamber pressures reach a nadir. For the right atrium, this occurs during late diastole and for the right ventricle during early diastole. With increasing pericardial pressure, the right and left ventricles compete for space resulting in the right ventricle filling at the expense of the left. During inspiration, the left ventricle has decreased available stroke volume because of decreased flow from extrapericardial veins and a left shifting of the interventricular septum. This results in compromise of stroke volume during inspiration and pulsus paradoxus in the peripheral circulation.

Cardiac compression from accumulation of pericardial fluid is a situation of many variables. One factor is the distensibility of the pericardial sac itself. Sometimes, accumulation of only a small amount of fluid or blood can result in cardiac tamponade. This situation can occur in cath lab or electrophysiology lab during procedures. Hemodynamic monitoring of systemic pressure may reveal inspiratory drop in blood pressure and indicate the presence of pericardial fluid. Echocardiography may show pericardial fluid and indicate the need for pericardiocentesis.

Interestingly, one of the functions of the pericardium is to contain the heart. When the heart dilates, the pericardium tends to limit diastolic expansion. This phenomenon is manifest when the pericardium is removed and diastolic volumes of the cardiac chambers increase. Sudden expansion of either ventricle in certain clinical situations can be harmful. For example, this becomes operative in the setting of pulmonary hypertension and pericardial effusion. Sudden removal of pericardial fluid can result in an even more dilated, thin-walled right ventricle, and hemodynamic deterioration can occur.

Doppler signs include exaggerated reciprocal changes in mitral and tricuspid Doppler inflow velocities. An inspiratory change in Doppler tricuspid inflow velocity of 60% is significant, whereas a reciprocal change in mitral Doppler inflow velocity of 30% is significant and indicates tamponade. In the presence of other conditions such as chronic obstructive lung disease, exaggerated inspiratory and expiratory velocities occur. Other abnormal ventricular filling patterns such as seen in atrial septal defect, aortic regurgitation, and pulmonary hypertension may alter these dynamics and make the diagnosis of cardiac compression challenging.³,⁴,⁵,⁶,⁷,⁸,⁹,¹⁰

Large amounts of pericardial fluid may cause the heart to swing from beat to beat, or this swinging may occur over several cardiac cycles. This causes the dramatic changes on the electrocardiogram that is called “electrical alternans.” This can occur on every other beat or with groups of beats depending on the amount of fluid that is present and the heart rate.