IS SODIUM-ACETATE DEXTRAN SUPERIOR TO SODIUM-CHLORIDE DEXTRAN FOR SMALL-VOLUME RESUSCITATION FROM TRAUMATIC HEMORRHAGIC-SHOCK

Small volumes (4 mL/kg body weight (bw)) of hypertonic sodium chloride dextran effectively restore cardiac output and nutritional blood flow and increase arterial pressure in severe hemorrhagic shock. It has be en suggested that the chloride anion be replaced with acetate to provi de a solution that avoids the risk of hyperchloremia and has the advan tage of supplying a buffering base to optimize hypertonic resuscitatio n. This study compares the effects of hypertonic sodium chloride dextr an solution (7.2% NaCl/10% dextran 60 [NaCl-Dx]; n = 7) with sodium ac etate dextran (10.4% Na-Ac/10% dextran 60 [NaAc-Dx]; n = 6) on hemodyn amic, oxygen transport, and metabolic variables. Both solutions had th e identical osmolality (2400 mOsmol/kg). Dogs (16.9 +/- 1.9 kg) were a nesthetized and mechanically ventilated. Shock was induced by exterior ization of intestine and blood withdrawal (50% of blood volume) to mai ntain mean arterial blood pressure (MAP) at 40 mm Hg for 75 min. There after, resuscitation was performed either with NaCl-Dx (4 mL/kg over 2 min) or NaAc-Dx (4 mL/kg over 4 min). During hypertonic resuscitation , there was a shortlasting decrease in MAP, which was more pronounced in the NaAc-Dx group (Delta MAP -7.3 +/- 2.5 mm Hg). Cardiac index and oxygen consumption were normalized within 5 min after resuscitation w ith both solutions. In NaAc-Dx-treated animals, MAP remained at lower values as compared to NaCl-Dx-treated dogs at 5 and 30 min after resus citation (52 +/- 3 vs 74 +/- 6, and 61 +/- 7 vs 79 +/- 12 mm Hg; P < 0 .05). Arterial pH (7.27 +/- 0.02 vs 7.17 +/- 0.06 at 5 min, 7.31 +/- 0 .04 vs 7.23 +/- 0.07 at 30 min, and 7.32 +/- 0.05 vs 7.26 +/- 0.05 at 60 min; P < 0.05) and bicarbonate concentrations (24.4 +/-: 2.1 vs 16. 7 +/- 9.5 at 5 min, 26.6 +/- 1.8 vs 18.0 +/- 1.9 at 30 min, and 27.5 /- 2.1 vs 19.1 +/- 1.7 mmol/L at 60 min; P < 0.05) in the plasma were normalized shortly after NaAc-Dx infusion; however, hyperlactemia pers isted after resuscitation with NaAc-Dx (7.10 +/- 1.48 vs 3.82 +/- 1.45 at 30 min, and 5.40 +/- 1.73 vs 2.71 +/- 0.89 mmol/L at 60 min; P < 0 .05). We conclude that NaAc-Dx offers no conclusive advantages as comp ared to NaCl-Dx for resuscitation from traumatic, hemorrhagic shock in our model of controlled hemorrhage. Although NaAc-Dx improved acid ba se status, hyperlactacidemia persisted.