Pericardiocentesis

Pericardium and Pericardial Space

The pericardium is a two-layered fibroelastic sac surrounding the heart. The pericardium is avascular but well innervated, so inflammation induces pain. The visceral pericardium is a single-cell layer that adheres to the epicardium. The outer parietal pericardium consists mostly of collagen with some elastin. These two layers create the pericardial space, which normally contains 15 to 50 mL of serous fluid and is under negative pressure to promote filling of the right ventricle (RV) during diastole. Pericardial fluid provides lubrication for cardiac contractility and acts as a “shock absorber” for deceleration forces.

The pericardium is a tense structure, but it also has some elasticity. These properties limit the amount of cardiac dilation that is possible during diastole and enhance mechanical interactions between the atria and ventricles during systole. This semi-elastic property can also tolerate an acute (i.e., over a period of hours to days) accumulation of pericardial fluid (80 to 120 mL) without significantly increasing intrapericardial pressure, which is the flat portion of the pressure-volume curve for pericardial pressure ( Fig. 16.1 ). Once a critical volume is reached, adding as little as 20 to 40 mL can double intrapericardial pressure (the steep portion of the pressure-volume curve [see Fig. 16.1 ]) and cause clinical decompensation from cardiac tamponade. Cardiac tamponade typically occurs with an intrapericardial pressure of 15 to 20 mm Hg.

Slow and chronic accumulation of pericardial fluid (over a period of weeks to months) causes the pericardium to expand circumferentially, and it can accommodate several liters of fluid with minimal alteration in intrapericardial pressure. Patients with this condition may be asymptomatic despite large effusions. No specific pericardial volume predicts the hemodynamic consequences of an effusion; such consequences depend on the acuity of the accumulation of the fluid.

Pathophysiology of Pericardial Tamponade

To generate an effective stroke volume, the left ventricle (LV) must be filled during diastole, and this process relies primarily on adequate filling of the RV. Normal inspiration makes the intrathoracic space more negative, which promotes RV filling by increasing venous return and causing dilation of the RV chamber secondary to a reduction in the tension in the RV free wall ( Video 16.1 ).

Elevated intrapericardial pressure (i.e., early tamponade) first results in abnormal RV filling followed by abnormal LV filling. In this situation, the free wall of the RV cannot expand against the pericardial fluid during inspiration. To accommodate RV filling, the interventricular septum bows abnormally into the LV, which reduces its volume; this is also known as ventricular interdependence. LV filling, stroke volume, and ultimately distal tissue perfusion is reduced. This phenomenon is responsible for pulsus paradoxus (PP; described later in this chapter), which is sometimes observed with tamponade. LV filling is also reduced by the collapse of right-sided structures. After a critical volume is reached on the pressure-volume curve (see Fig. 16.1 ), the intrapericardial pressure is transmitted to the inferior vena cava (IVC) and right atrium. These thin-walled structures then become compressed and reduce filling of the RV.

The atria and pulmonary circulation are at much lower pressure than systemic arterial pressure and are also vulnerable to rising intrapericardial pressure ( Fig. 16.2 ). Late in tamponade a “pressure plateau” occurs in which right atrial pressure, RV diastolic pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure are virtually identical. This equalization of chamber pressure leads to a reduction in venous return and the echocardiographic hallmark of tamponade: diastolic collapse of the RV (discussed later in this chapter). At this point, hemodynamic collapse is imminent, with severe hypotension, and potentially pulseless electrical activity (PEA) developing. Unless intrapericardial pressure is decreased immediately, cardiac arrest will ensue.

Compensatory Mechanisms and Pericardiocentesis

To maintain a physiologic cardiac output early in tamponade, the sympathetic nervous system increases the heart rate, arterial vasoconstriction (to maintain mean arterial blood pressure), and venoconstriction (to maintain normal venous-atrial and atrioventricular filling gradients). Early in tamponade, these compensatory mechanisms are usually effective in maintaining adequate cardiac output.

Compensatory mechanisms also preserve normal cardiac contractility and myocardial perfusion. However, when the pericardial pressure overwhelms the compensatory mechanisms, coronary perfusion pressure is reduced, which leads to myocardial ischemia, systolic dysfunction, and ultimately a reduction in cardiac output. Experimental induction of severe tamponade demonstrated microscopic ischemic cardiac injury. Lactic acidosis (resulting from reduced cardiac output and systemic hypoperfusion) also leads to further reduction in cardiac contractility and, ultimately, cardiac output.

Removal of pericardial fluid (i.e., pericardiocentesis) reverses the pathophysiologic processes just described by improving coronary filling, cardiac filling, and hence cardiac output. Interestingly, the pressure-volume relationship of the pericardial space demonstrates hysteresis; that is, withdrawing a certain quantity of fluid reduces intrapericardial pressure more than addition of the same amount of fluid increases intrapericardial pressure. This effect, however, is not universal and may vary among patients and in various disease states ( Fig. 16.3 ).

Special Considerations in Patients With Pericardial Effusion and Tamponade

Under normal circumstances, positive pressure ventilation (e.g., mechanical ventilation) reduces venous return to the right side of the heart by increasing intrathoracic pressure. This could be detrimental for patients with tamponade because right-sided filling is already compromised and further reductions can lead to severe hemodynamic instability. Therefore positive pressure ventilation (i.e., noninvasive or invasive) should be avoided in patients with known or suspected tamponade unless it is absolutely necessary (e.g., respiratory failure).

Low-pressure pericardial tamponade is defined as a hemodynamically significant effusion with an intrapericardial pressure that is lower than expected. This category of tamponade occurs in patients with subacute or chronic effusions, but present with a superimposed hypovolemia (e.g., associated with long-term diuretic use, dehydration, or excessive dialysis). The diagnosis may be challenging because the classic symptoms and findings on physical examination (e.g., distended neck veins) may be absent. Ultrasound is most helpful in making the diagnosis in these patients. Fluid boluses may temporize the hemodynamic compromise while pericardial decompression is being arranged.

Acute Hemopericardium

Acute hemopericardium, or rapid accumulation of blood in the pericardial space, can have a traumatic or nontraumatic etiology. It is one of the most feared causes of tamponade because the semi-elastic pericardium cannot accommodate acute increases in pericardial fluid and clinical deterioration can be rapid. This diagnosis can be challenging to make because there may be little or no evidence during the initial evaluation (e.g., pericardial size might be normal on a chest radiograph). Common causes include trauma and aortic dissection retrograde into the pericardial sac.

Nonhemorrhagic Effusions

Nonhemorrhagic pericardial effusions usually accumulate slower than acute hemopericardium does (over a period of weeks to months). Chronic fluid accumulation allows the pericardium to stretch circumferentially and accommodate up to 2000 mL of fluid without any hemodynamic compromise. Effusions that grow slowly allow the circulatory system to adapt to increased intrapericardial pressure, thereby further maintaining hemodynamic stability. Thus, asymptomatic patients with moderate to large effusions may not need emergency pericardiocentesis, in contrast to patients with acute hemopericardium.

Nonhemorrhagic effusions have several causes (see Box 16.1 ), and the exact one may not be obvious during the initial evaluation without diagnostic pericardiocentesis. Common causes of nonhemorrhagic effusions are discussed in the following sections.