Hemodynamic adaptation to acute myocardial contusion complicating blunt chest injury.

The immediate hemodynamic sequelae of blunt chest injury complicated by acute myocardial contusion were examined in multiply traumatized patients. Focal defects of ventricular wall motion defined by gated cardiac scintigraphy identified acute myocardial contusion in 28 of 43 patients, involving the right ventricle alone in 18 (group 1A), the left ventricle in 4 (group 1B) and both ventricles in 6 (group 1C). Qualitatively normal ventricular wall motion was found in the 15 patients (group 2). Although there was no difference between groups 1A and 2 in mean systemic oxygen transport (620 +/- 189 vs 627 +/- 105 ml/min/m2), left ventricular ejection fraction (52 +/- 14% vs 60 +/- 9%) or calculated left ventricular end-diastolic and end-diastolic and end-systolic volumes, mean right ventricular (RV) ejection fraction was significantly lower in group 1A (29 +/- 9%) than in group 2 (47 +/- 7%, p less than 0.01). Concomitantly, evidence of RV systolic dysfunction was ml/m2) but not in group 2 (RV end-systolic volume, 50 +/- 21 ml/m2, p less than 0.05). RV stroke work was similar between the groups, and RV pump function was identical by virtue of a larger RV preload in group 1A (RV end-diastolic volume 143 +/- 63 ml/m2) than in group 2 (RV end-diastolic volume 93 +/- 26 ml/m2, p less than 0.05). Thus, use of the RV Frank-Starling mechanism in patients with traumatic RV contusion maintains RV pump function at a level similar to that in traumatized patients without acute myocardial contusion.