Pericardial effusion and cardiac tamponade

Cardiac tamponade results from an increase in pericardial pressure that is sufficient to impede cardiac filling, resulting in high venous filling pressures, low cardiac output, and end-organ hypoperfusion. Most often this is due to the accumulation of a pericardial effusion though there are other possible causes. Patients usually present with features of cardiogenic shock, though some may initially be normotensive or hypertensive. Echocardiography can diagnose the presence of pericardial disease, especially pericardial effusion. Any associated haemodynamic sequelae can often be inferred by static and dynamic two-dimensional echocardiographic and Doppler measured intracardiac flow velocity abnormalities. These include atrial and ventricular wall inversion or collapse, and increased respiratory phasic flow velocities in tricuspid and mitral inflow. The concepts of transmural pressure, pericardial restraint, interventricular dependence, and cardiorespiratory interactions underpin the understanding and limitations of these echocardiographic findings. However, the impact of positive pressure ventilation remains problematic with respect to the interpretation of Doppler-derived intracardiac flow velocity variation. Echocardiography can also identify conditions that may confound the interpretation of accepted echocardiographic criteria (e.g. right ventricular hypertrophy, hypovolaemia, isolated chamber compression after cardiac surgery) and diagnose conditions that may mimic or exaggerate tamponade pathophysiology such as large compressive pleural effusion. Finally, echocardiographic criteria can aid stratification of the risk of tamponade in patients with pericardial effusion, and if necessary, guide percutaneous pericardiocentesis.