When pericardial fluid accumulates, the compliance of the parietal pericardium initially increases, resulting in a stable intrapericardial pressure. When the pericardial reserve volume is exceeded, pericardial compliance begins to fall and the intrapericardial pressure rises, and the central venous pressure must increase to maintain a gradient that allows cardiac filling. When the stretch threshold of the pericardium is exceeded, pericardial compliance markedly decreases, resulting in rapid increases in pericardial pressure with increasing volume (Fig. 7.3). At this point, the intrapericardial pressure may first equalize with the right ventricular diastolic pressure, and then with the left ventricular diastolic pressure. Critical tamponade occurs when all cardiac chambers have equal diastolic pressure. At this inflection point, there is collapse of the right-sided cardiac chambers and the cardiac output can suddenly drop (Fig. 7.3). Circulation at this point is maintained only through an increase in heart rate, contractility, and peripheral arteriolar vasoconstriction. Left untreated, this can result in circulatory failure and death [13].

The rate of accumulation of pericardial fluid and the total fluid volume determine the relative hemodynamic impairment caused by excess fluid in the pericardial space (Fig. 7.3). Conditions like uremic pericarditis or malignancy-related effusion can cause gradual accumulation of a large volume (>2 L) of fluid in the compliant pericardium, potentially causing minimal symptoms and no hemodynamic effects. However, in acute conditions, such as cardiac free wall rupture from pacemaker lead placement, rapid accumulation of even small amounts of pericardial fluid (50–80 mL) can exceed the pericardium’s ability to stretch and can cause hemodynamic compromise [14].

As the pericardial pressure exceeds the central venous and pulmonary venous pressure, diastolic filling is impaired and becomes increasingly influenced by the respiratory variation in intrathoracic pressures. During inspiration, as the intrathoracic pressure becomes more negative, central venous blood flow to the right atrium and right ventricle (RV) is augmented; at the same time, there is pooling of blood in the pulmonary veins, thereby reducing flow to the left atrium. As the RV is preferentially filled during inspiration, the interventricular septum bows into the left ventricle (LV), causing a drop in cardiac output and hence a drop in blood pressure with inspiration (Fig. 7.4). The opposite holds true with expiration, when the intrathoracic pressure increases and causes diminished return of blood from the vena cava to the right side of the heart and increased flow from the pulmonary veins into the left side of the heart. As more blood is accommodated in the LV, the ventricular septum bows toward the RV. This over-filling and under-filling of the heart with respect to respiration forms the basis for “pulsus paradoxus,” a classic clinical finding associated with cardiac tamponade. Although not specific for cardiac tamponade, an inspiratory drop in blood pressure of more than 10 mmHg in patients with pericardial effusion has a pooled sensitivity of 82 % for cardiac tamponade [13]. Moreover, the severity of the pulsus paradoxus correlates with the severity of hemodynamic compromise in cardiac tamponade [15]. However, caution should be used when interpreting this finding in patients with severe obstructive lung disease, severe volume depletion, right or left ventricular hypertrophy, or in those on invasive positive pressure ventilation. The clinician must be cognizant that cardiac tamponade is a clinical diagnosis and that neither presence of an elevated pulsus paradoxus nor an echocardiography finding of a pericardial effusion establishes the diagnosis of tamponade.

The cardiac and pericardial structures must be visualized in multiple echocardiographic views to confidently rule out the presence of a pericardial effusion. The pericardial layers appear as a thin, bright, echogenic line around the myocardium (Fig. 7.6). The normal thickness of the pericardium is 1–2 mm. In the normal pericardium, there is less than 25 mL of serous fluid in the pericardial sac formed by the visceral and parietal pericardium. A simple pericardial effusion is visualized as an anechoic (black) area on B-mode, contiguous to the adjacent cardiac structures and separating the echogenic layers of the pericardium (Fig. 7.7). With advanced practice, M-mode and pulsed wave Doppler can be utilized to assess for findings of cardiac tamponade.