The pericardium is composed of visceral and parietal components. The visceral pericardium is a serosal monolayer that adheres firmly to the epicardium, reflects over the origin of the great vessels, and together with a tough, fibrous parietal layer, envelops the heart.10 The pericardial space enclosed between the two serosal layers normally contains up to 50 mL of plasma ultrafiltrate, and a pericardial effusion is considered to be present when accumulated fluid within the sac exceeds this amount.10 Cardiac tamponade is characterized by hemodynamic instability due to heart compression by the accumulation of fluid, blood, clots, or gas in the pericardial space.1
The pericardium may be affected by all categories of diseases, including infectious, autoimmune, neoplastic, iatrogenic, traumatic, and metabolic1. Pericardial effusions may develop rapidly (acute) or more gradually (subacute, when less than 3 months; or chronic, when longer than 3 months).10 If fluid accumulation is gradual, pericardial pressure remains low because the pericardium can increase its compliance by undergoing stretch, which is accomplished by an increase in surface area and mass.5 With continued accumulation of fluid, the intrapericardial pressure eventually increases and becomes high enough to impede cardiac filling—at which time, cardiac function becomes impaired and cardiac tamponade can be considered to be present.10
The true incidence of cardiac tamponade is difficult to estimate, but pericardial diseases likely to progress to tamponade include some infectious diseases (e.g., human immunodeficiency virus infection or tuberculosis), malignancies, renal failure, trauma/iatrogenic, and hemopericardium in aortic dissection and rupture of the heart after acute myocardial infarction.12 At postmortem, cardiac tamponade is most often related to hemopericardium, attributable to either ruptured acute myocardial infarction or dissecting aortic aneurysm.14
Pericardial effusions are often discovered incidentally during evaluation of other cardiopulmonary diseases; indeed, the majority of patients have no symptoms specific to the effusion.10 Electrocardiography may show signs of large pericardial effusion, with especially low QRS voltage and electrical alternans,4 which is an electrocardiographic phenomenon defined as an alternating amplitude or axis of the QRS complexes in any or all leads. Less commonly, compression of the adjacent intrathoracic structures results in hoarseness, hiccough, and nausea.1
Cardiac tamponade often presents as a cardiogenic obstructive shock with shortness of breath, tachycardia, hypotension with a narrow pulse pressure (but blood pressure may be preserved in some cases),2 and pulsus paradoxus (an inspiratory fall of systolic blood pressure of more than 10 mmHg during normal spontaneous breathing), which is an important diagnostic finding in CT.7 Jugular venous distention, marked hypotension, and muffled heart sounds (Beck’s triad) are the three classic signs of cardiac tamponade.
Echocardiography is the main diagnostic method for detection of pericardial effusion and tamponade.4 The transthoracic approach is often sufficient, but the transesophageal route must be preferred in intubated patients following trauma or cardiac surgery in whom loculated or extrapericardial tamponade may result in nonspecific clinical presentation.9 The main echocardiographic sign of cardiac tamponade is heart collapse. It mainly occurs in low-pressure cardiac chambers with thin walls—namely the right atria at end-diastole (early sign, very sensitive, but poorly specific unless sustained at least one-third of the cardiac cycle),8 and the right ventricle outflow tract at early diastole (late sign, very specific);3 left atrium and left ventricle collapses are less common because intra-cavitary pressures are higher.4 The heart collapse is enhanced during the spontaneous expiratory phase, because of the decreased venous return; conversely, it may be mitigated by hypervolemia, pulmonary hypertension, and right ventricle hypertrophy.13
Two of the most common treatments for severe pericardial effusion and cardiac tamponade are pericardiocentesis and pericardiectomy. The choice between the two are based on patient presentation, severity, and provider comfort and experience. Pericardiocentesis can be performed under fluoroscopic or echocardiographic guidance.10 Real-time echocardiography guidance with microbubbles injection can be used by experienced staff for safe bedside pericardiocentesis.15 In the largest published series, the para-apical location was utilized in two-thirds, while the subxiphoid location was ideal in only 15%.11 In an emergency, a blind approach has been used to successfully perform a pericardiocentesis when ultrasound was not available.
Surgical pericardiectomy and drainage, though less commonly performed than pericardiocentesis, is often preferred when the pericardial effusion has reaccumulated or is loculated, biopsy of the pericardium is desired, or the patient has a coagulopathy.10 Surgical drainage is preferable in some cases like purulent pericarditis or bleeding (e.g., type A aortic dissection, ventricular free wall rupture).12 In some patients presenting with cardiac tamponade and large pleural effusion, drainage of the pleural effusion may be given priority.6
Despite substantial progress in the detection, quantification, characterization, management, and prognosis of pericardial diseases, and the recent guidelines and recommendations, there is only limited evidence-based data to guide the management of pericardial effusion and cardiac tamponade.10 Echocardiography remains critical for recognition and management of pericardial effusions and their hemodynamic sequelae, but when complex effusions are present or echocardiographic imaging is suboptimal, multimodality imaging is essential.10