Response of the heart to nonpenetrating cardiac trauma

The purpose of this investigation was to study the acute effects of blunt cardiac trauma upon left ventricular (LV) function. In 34 open-chest anesthetized dogs, direct impact to the anterior surface of the heart was produced by an air-pressurized impactor at 12 m/sec in 15 dogs and at 18 m/sec in 19 dogs. Impact displacement was limited to 2 cm. Seventeen dogs (50%) died of arrhythmias within a few minutes of impact. In nine surviving dogs impacted at 12 m/sec, there was an immediate reduction of LV function following impact. At 5 minutes following impact this reduction of LV function was characterized by a 19% reduction of cardiac output, 35% reduction of maximal isovolumic LV rate of change of pressure (dp/dt), a 12% reduction of peak aortic flow, and a 23% reduction of peak rate of change of flow. These indices of ventricular performance returned nearly to control levels 60 to 90 minutes following impact. In eight surviving dogs that experienced impact at 18 m/sec, impairment of LV function was greater in the immediate impact period following impact and impaired function remained throughout the 90-minute duration of observation. Autopsy of all dogs showed cardiac contusion. Following the more severe impact, contusions were more extensive and involved the left ventricular endocardial surface and intraventricular septum as well as the epicardial surface. Parallel changes, therefore, of the extent of pathologic changes and the extent of functional impairment were observed. Animals that survived the potentially fatal arrhythmias immediately after impact showed functional impairment of the heart that was only moderate and compatible with life.