BACKGROUND: Prior functional studies on myocardial contusion (MC) have emphasized left ventricular performance even though the right ventricle (RV) is more likely to be injured after blunt trauma. Furthermore, associated injuries requiring resuscitation and surgery are frequently present. Our aim was to evaluate the impact of MC on RV function after MC and subsequent resuscitation from hemorrhagic shock. METHODS: RV performance was evaluated with a modified pulmonary artery catheter that determines RV volumes and ejection fraction (RVEF), as well as filling pressures and cardiac output in an anesthetized swine model. RESULTS: MC caused a 28% fall in mean arterial pressure and a 33% decrease in cardiac output. RVEF was 82%, and RV stroke work was 49% of baseline after injury. Resuscitation of hemorrhagic shock to baseline preload or greater failed to restore mean arterial pressure or cardiac output (depressed 23% and 22%, respectively). RV end-diastolic volume returned to baseline and central venous pressure was increased. RV dysfunction was depicted by a sustained depression of RV stroke work and RVEF. CONCLUSIONS: Impaired RV compliance and contractility, which was evident throughout this study, may hamper resuscitative efforts after multiple blunt trauma. RV monitoring may be useful in this setting.
BACKGROUND: Prior functional studies on myocardial contusion (MC) have emphasized left ventricular performance even though the right ventricle (RV) is more likely to be injured after blunt trauma. Furthermore, associated injuries requiring resuscitation and surgery are frequently present. Our aim was to evaluate the impact of MC on RV function after MC and subsequent resuscitation from hemorrhagic shock. METHODS: RV performance was evaluated with a modified pulmonary artery catheter that determines RV volumes and ejection fraction (RVEF), as well as filling pressures and cardiac output in an anesthetized swine model. RESULTS: MC caused a 28% fall in mean arterial pressure and a 33% decrease in cardiac output. RVEF was 82%, and RV stroke work was 49% of baseline after injury. Resuscitation of hemorrhagic shock to baseline preload or greater failed to restore mean arterial pressure or cardiac output (depressed 23% and 22%, respectively). RV end-diastolic volume returned to baseline and central venous pressure was increased. RV dysfunction was depicted by a sustained depression of RV stroke work and RVEF. CONCLUSIONS: Impaired RV compliance and contractility, which was evident throughout this study, may hamper resuscitative efforts after multiple blunt trauma. RV monitoring may be useful in this setting.