Cardiac tamponade is a clinical syndrome resulting from the accumulation of fluid in the pericardial space resulting in reduced ventricular filling and subsequent cardiovascular compromise. The diagnosis of cardiac tamponade is made clinically, not with imaging. Imaging such as echocardiography; however, can help aid in, and confirm, the diagnosis. There are classically 3 phases of developing tamponade. Phase I is fluid accumulation leading to increased stiffness of the ventricle. A higher filling pressure is needed due to the stiffness. Left and right ventricular pressures are higher than the pericardial pressure in this phase. In phase II, pericardial pressure increases above the ventricular pressures as further fluid accumulates. This leads to decreased cardiac output. Phase III is characterized by a further reduction in cardiac output as the pressures in the ventricles and pericardium equilibrate.
The underlying physiologic mechanism for the development of tamponade is a significant reduction in diastolic filling. This is caused by the increasing intrapericardial pressures that cause the distending pressure of the ventricles to become insufficient. Tachycardia is the initial compensatory response to these hemodynamic changes. Venous return is also compromised due to the compression of the heart resulting in right atrial and right ventricular collapse. Prompt diagnosis is crucial as this disease process is universally fatal if left untreated. The most common symptoms are tachycardia, dyspnea, and elevated jugular venous pressure. Important echocardiographic findings are an effusion and early diastolic collapse of the right ventricle. Key to the diagnosis is the identification of respiratory variation.
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Defined by: Patrick Kinnebrew, MD