Pathophysiology

Normally, the pericardial space contains up to 50 mL of fluid. However, cancerous cells can invade this space via direct invasion or through blood or lymphatic metastasis, leading to substantial malignant fluid accumulation. An acute increase of only 200 mL of fluid may cause a steep increase in intrapericardial pressure, impairment of cardiac filling, and hemodynamic compromise.5 However, patients with chronic pericardial disease can have stress relaxation, whereby, over the course of weeks or months, the pericardium may accommodate up to 2 L of fluid, without a significant increase in intrapericardial pressure.5

Signs and Symptoms

The presenting complaints associated with malignant pericardial effusions can be nonspecific, ranging from exertional dyspnea to tachycardia and chest pain. The classic Beck triad6 of muffled heart sounds, hypotension, and increased jugular venous pressure is seen in one-third of patients with rapidly accumulating effusions7 but is less common in patients with chronic effusions. Pulsus paradoxus (Box 1), characterized by a decrease in systolic blood pressure of more than 10 mm Hg with inspiration, is observed in up to 77% of patients with pericardial tamponade.6

Diagnosis

Pericardial tamponade is usually diagnosed with echocardiography. Findings that help to differentiate pericardial effusion from cardiac tamponade are right atrial collapse in late diastole and right ventricular collapse in early diastole. Right atrial collapse is a more sensitive marker of pericardial tamponade, whereas right ventricular collapse is more specific.8 Doppler findings suggestive of increased intrapericardial pressure are changes of more than 30% in the mitral inflow velocities and more than 50% in the tricuspid inflow velocities. A respirophasic shift in the interventricular septum indicates that the right heart expands during inspiration at the expense of left heart filling.9

Other diagnostic modalities may also identify pericardial tamponade. Electrocardiographic findings suggestive of pericardial effusion and tamponade include low-amplitude waveforms and electrical alternans.4 On chest radiography, a sudden increase in the transverse cardiac diameter, termed a water bottle heart, suggests a rapidly accumulating pericardial effusion.7 Computed tomographic (CT) imaging can also aid in the diagnosis.8 Cardiac catheterization shows increased right-sided pressures and equalization of the right atrial, right ventricular, and pulmonary capillary wedge pressures.8,9

Management

Initial management with fluid resuscitation is appropriate in patients who seem to be hypovolemic and hemodynamically unstable. However, fluid administration could be detrimental to euvolemic or hypervolemic patients by increasing intracardiac pressure and thus compromising coronary perfusion pressure.8,9 The role of inotropes in the management of tamponade remains unclear.

The definitive treatment of acute pericardial tamponade is emergent pericardiocentesis. Preferably, this treatment is performed using ultrasound guidance. Almost half of malignant pericardial effusions may reaccumulate,10 and thus, placement of an indwelling catheter should be considered at the time of pericardiocentesis. A pericardial window can also provide long-term symptomatic relief in select cases.11,12 Patients with tamponade are dependent on preload as well as changes in the intrathoracic pressure. Procedures such as endotracheal intubation may further reduce preload and afterload both because of positive pressure and induction agents. Routine prophylactic intubation is not recommended for tamponade, because of the risk of cardiac arrest during or shortly after intubation. Careful consideration of the risks and benefits should be considered if intubation is contemplated.

Prognosis

Despite adequate treatment, the long-term prognosis for patients with malignant pericardial involvement remains poor. Median life expectancy is about 5 months after the diagnosis of a malignant pericardial effusion. Hemodynamic instability, dependence on pressors, and a higher volume of pericardial drainage are poor prognostic markers.13 Clinical features and management are summarized in Table 1.