The purpose of this study was to explore the possibility that nonpenetrating cardiac impact can directly result in hepatic and splenic injury through hemodynamic effects. Impact upon the anterior surface of the heart was produced in 34 open-chest anesthetized dogs. In 15 dogs the velocity of impact was 12 m/sec and in 19 dogs it was 18 m/sec. Pressure in the inferior vena cava transiently reached 194 ± 25 mm Hg in the dogs impacted at 12 m/sec and 377 ± 44 mm Hg in dogs impacted in 18 m/sec. Aortic pressure transiently reached 449 ± 32 mm Hg in dogs impacted at 12 m/sec and 682 ± 33 mm Hg in dogs impacted at 18 m/sec. Gross capsular lacerations of the liver occurred in six dogs (18%) following cardiac impact. All dogs showed hepatic congestion and most showed microscopic injury of liver cords, central veins, and portal tracts. Dogs that survived cardiac impact for the duration of observation (90 minutes) showed focal acute inflammation of liver triads and hepatic sinusoids, indicating a more subtle degree of injury. The spleens of eight dogs showed areas of grossly visible subcapsular hemorrhage. Subcapsular congestion of the spleen occurred in almost all dogs. This study shows therefore that nonpenetrating cardiac impact may result in hepatic and splenic injury. A likely mechanism may be the extraordinarily high venous pressure that develops at the instant of impact, although transient striking elevations of arterial pressure may also contribute.