Cardiac tamponade is defined as a decompensated form of cardiac compression caused by the accumulation of pericardial effusion and rising intrapericardial pressure.1 Cardiac tamponade may complicate any medical condition associated with pericardial effusion, although it is not synonomous with a large pericardial effusion and has its own specific diagnostic criteria based on hemodynamic and echocardiographic signs. Cardiac tamponade causes obstructive shock and should be regarded as a medical emergency. Medical professionals in the disciplines of surgery, internal and emergency medicine should be familiar with the pathophysiology, clinical presentation, and natural progression of cardiac tamponade to avoid delays in the evaluation and management of this life-threatening condition. Echocardiography is an essential tool for the diagnosis of cardiac tamponade and the evacuation of pericardial fluid. Bedside echocardiography is often performed by intensivists as a part of point of care ultrasonography of critically ill patients; therefore, the recognition of the echocardiographic features of cardiac tamponade is essential for the critical care provider.
In a healthy individual, pericardial pressure is lower than atmospheric pressure and essentially equates to negative intrathoracic pressure. While the pericardium expands to accommodate fluid accumulation over a long period of time, the pericardial space remains constant and fixed at any particular moment. Thus, during systole, pericardial pressure becomes more negative due to the rapid reduction in ventricular size. The lower pericardial pressure combined with the forward flow of blood generated by systolic ventricular contraction contribute to increased venous return to the atria. During diastole pericardial pressure increases due to ventricular expansion, which creates a pressure gradient between the atria and ventricles propelling blood forward and defines a rapid filling diastolic phase. Atrial contraction completes ventricular filling during diastole. Cardiac tamponade occurs when pericardial pressure reaches the point at which diastolic pressures in the cardiac chambers equilibrate, atrioventricular and interventricular “competition” for filling volumes occurs and hemodynamic compromise results.2–4
First, in late diastole, pericardial pressure exceeds central venous and atrial pressures causing right atrium and caval veins to collapse, thus decreasing right ventricular filling volume. Left atrial collapse is observed in approximately 25% of patients and is a very specific sign of cardiac tamponade.5 When right ventricular contraction occurs, pericardial pressure decreases and relieves right atrial compression. As pericardial fluid accumulates and the intrapericardial pressure continues to rise, even slight additional pressure increases during early diastole cause the right atrium and ventricle to collapse.4 The duration of right atrial collapse at >30% of the cardiac cycle and early diastolic RV collapse both have high specificity (>80%) for cardiac tamponade.6
Interventricular competition appears more prominent as a function of the respiratory cycle. During inspiration, intrathoracic pressure decreases (becomes more negative), accelerating blood flow to the right-sided cardiac chambers. Because pericardial pressure is substantially elevated in the setting of cardiac tamponade, the right ventricle accommodates additional blood volume by invaginating the interventricular septum (IVS) ...