Two-dimensional echocardiography enabled the direct visualization of a rare and unusual sequelae of blunt anterior chest trauma: the formation of a localized anterior mediastinal hematoma causing extrapericardial cardiac tamponade. The visualization of a Swan-Ganz catheter in the twodimensional echocardiogram aided in confirming the location of both the obliterated right ventricular chamber and the right ventricular outflow tract posterior to the mass. The combination of decreasing cardiac output without evidence of myocardial dysfunction and the similarity of central venous pressure and pulmonary capillary wedge pressure suggested significant cardiac tamponade.
Due to variability in the size, location, and rate of formation of a hematoma in the mediastinum, hemodynami-cally significant impairment of cardiac output may occur without all the expected signs of intrapericardial tamponade. It is particularly unusual, in this specific instance, for blood to collect in the anterior mediastinal space and encroach upon one or more of the cardiac chambers. Often, these collections vent via paths of least resistance to either the pleural spaces or the retroperitoneum via the diaphragmatic hiatus. Venous bleeding in this space should not produce a right ventricular collapse, but it is conceivable that a combination of venous filling and arterial hemorrhage from the sternal fractures encouraged accumulation of blood at higher pressures, causing encroachment on the right ventricle. This mass effect was “focal” rather than the global compression usually associated with cardiac tamponade, and therefore, did not present with pulsus pardoxus. This atypical form of cardiac tamponade can be compared with a loculated pericardial effusion or hematoma, and the affected chambers in turn determine the degree of hemodynamic embarass-ment and the presence or absence of typical clinical signs of tamponade. Source
In experimental production of tamponade using an inflatable balloon in dogs, Carey and associates demonstrated a greater incremental fall in cardiac output when the right ventricle was selectively compressed when compared to the left ventricle. In subsequent experimental compression of selected heart chambers, Fowler and Sabel constructed pockets within the pericardium over each chamber. When each compartment was filled selectively, the authors confirmed the hypothesis that right atrial and vena cava compression produce more significant hemodynamic compromise than compression of either ventricle.