HYPERTONIC SALINE-DEXTRAN RESUSCITATION FROM HEMORRHAGIC-SHOCK INDUCES TRANSIENT MIXED ACIDOSIS

Objective: To evaluate the magnitude and mechanism of potential metabo lic acidosis after resuscitation with 7.5% sodium chloride/ 6% dextran -70. Design: Blinded, randomized, control trial. Setting: Laboratory s etting. Subjects: Sixteen healthy Yorkshire swine. Interventions: Anes thetized, mechanically ventilated swine underwent 90 mins of hemorrhag ic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lacti c acid infusion (1.5 to 2.4 mmol/kg) was given during the last 60 mins of hemorrhage to produce pretreatment acidosis. The pigs were then gi ven either 4 mL/ kg of intravenous normal saline (n = 8) or 7.5% sodiu m chloride/6% dextran-70 (n = 8). Groups then received isotonic lactat ed Ringer's solution to restore and maintain cardiac output for 120 mi ns. Measurements and Main Results: There was no difference between gro ups during baseline or shock for any parameter. At the end of shock, a rterial pH and base balance were below baseline values. During resusci tation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a signif icant but transient decrease in arterial pH (from 7.407 +/- 0.015 to 7 .339 +/- 0.025) and base balance (from -6.5 +/- 0.7 to -9.9 +/- 1.0 mm ol/L). These changes returned to shock levels by 10 mins and then norm alized to baseline levels. Hypertonic saline/dextran resulted in an im mediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium m inus chloride concentrations), and no immediate change in anion gap. T he normal saline group did not show an initial transient decrease in p H and base balance during resuscitation. Plasma lactate, total protein , and hemoglobin concentrations decreased equally in both groups, alth ough they decreased more quickly with hypertonic saline/dextran. CO, t emporarily and insignificantly increased in arterial blood slightly mo re after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hype rtonic saline/dextran, while pH, base balance, and protein were decrea sing below shock values in animals initially treated with normal salin e. Conclusions: Hypertonic saline/dextran caused an immediate, transie nt acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic stro ng ion difference, but which was partially due to a mild transient res piratory acidosis. The acidemia was transient because of the offsettin g alkalotic effects of decreasing serum protein, normalization of elec trolytes, and transient nature of the increase in CO,. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status ap peared to be improved more effectively with hypertonic saline/ dextran than with isotonic saline resuscitation.