Ryukoh Ogino1. 1. Department of Acute Medicine, Kawasaki Medical School, Kurashiki, Okayama, Japan. qqryukoh@xa2.so-net.ne.jp
Abstract
BACKGROUND: A bolus of 7.5% NaCl-6% Dextran 70 (HSD) is effective in resuscitating hypovolemic shock. Common hemodynamic findings with HSD are restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. However, the effect of HSD upon cardiac function is still controversial. In our previous study, when HSD did not improve cardiac contractility, it was speculated that it might affect cardiac diastolic function without a change in contractility. Therefore, we studied the effects of HSD on cardiac diastolic function. METHODS:Hemorrhagic shock was created by exsanguination of 31.4 +/- 0.9 ml/kg (NS group) or 29.0 +/- 3.6 ml/kg (HSD group). Then mean BP was maintained at 50 mm Hg for 30 min in both groups. The HSD group (n = 6) received HSD (4 ml/kg) and the NS (control) group (n = 5) received normal saline (40 ml/kg) after the shock. Cardiac diastolic functions were measured in both groups using the peak negative dP/dt and the left ventricular end-diastolic pressure-volume relationship (EDPVR) during the experimental period: before shock, immediately, and 2 h after resuscitation. RESULTS:Hemodynamic parameters in both groups demonstrated similar changes throughout the experimental period. The peak negative dP/dt, stiffness constant, and elasticity obtained by EDPVR did not differ significantly between the two groups. CONCLUSION:HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume of HSD required to maintain circulation is significantly smaller than that of normal saline. However, our data revealed that HSD does not change cardiac diastolic function after hemorrhagic shock.
RCT Entities:
BACKGROUND: A bolus of 7.5% NaCl-6% Dextran 70 (HSD) is effective in resuscitating hypovolemic shock. Common hemodynamic findings with HSD are restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. However, the effect of HSD upon cardiac function is still controversial. In our previous study, when HSD did not improve cardiac contractility, it was speculated that it might affect cardiac diastolic function without a change in contractility. Therefore, we studied the effects of HSD on cardiac diastolic function. METHODS:Hemorrhagic shock was created by exsanguination of 31.4 +/- 0.9 ml/kg (NS group) or 29.0 +/- 3.6 ml/kg (HSD group). Then mean BP was maintained at 50 mm Hg for 30 min in both groups. The HSD group (n = 6) received HSD (4 ml/kg) and the NS (control) group (n = 5) received normal saline (40 ml/kg) after the shock. Cardiac diastolic functions were measured in both groups using the peak negative dP/dt and the left ventricular end-diastolic pressure-volume relationship (EDPVR) during the experimental period: before shock, immediately, and 2 h after resuscitation. RESULTS: Hemodynamic parameters in both groups demonstrated similar changes throughout the experimental period. The peak negative dP/dt, stiffness constant, and elasticity obtained by EDPVR did not differ significantly between the two groups. CONCLUSION:HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume of HSD required to maintain circulation is significantly smaller than that of normal saline. However, our data revealed that HSD does not change cardiac diastolic function after hemorrhagic shock.