Impact of Plasma-Lyte pH 7.4 on acid-base status and hemodynamics in a model of controlled hemorrhagic shock.

OBJECTIVE: Intravenous infusion of crystalloid solutions is a cornerstone of the treatment of hemorrhagic shock. However, crystalloid solutions can have variable metabolic acid-base effects, perpetuating or even aggravating shock-induced metabolic acidosis. The aim of this study was to compare, in a controlled volume-driven porcine model of hemorrhagic shock, the effects of three different crystalloid solutions on the hemodynamics and acid-base balance. METHODS: Controlled hemorrhagic shock (40% of the total blood volume was removed) was induced in 18 animals, which were then treated with normal saline (0.9% NaCl), Lactated Ringer's Solution or Plasma-Lyte pH 7.4, in a blinded fashion (n = 6 for each group). Using a predefined protocol, the animals received three times the volume of blood removed. RESULTS: The three different crystalloid infusions were equally capable of reversing the hemorrhage-induced low cardiac output and anuria. The Lactated Ringer's Solution and Plasma-Lyte pH 7.4 infusions resulted in an increased standard base excess and a decreased serum chloride level, whereas treatment with normal saline resulted in a decreased standard base excess and an increased serum chloride level. The Plasma-Lyte pH 7.4 infusions did not change the level of the unmeasured anions. CONCLUSION: Although the three tested crystalloid solutions were equally able to attenuate the hemodynamic and tissue perfusion disturbances, only the normal saline induced hyperchloremia and metabolic acidosis.

Impact of Plasma-Lyte pH 7.4 on acid-base status and hemodynamics in a model of controlled hemorrhagic shock

OBJECTIVE: Intravenous infusion of crystalloid solutions is a cornerstone of the treatment of hemorrhagic shock. However, crystalloid solutions can have variable metabolic acid-base effects, perpetuating or even aggravating shock-induced metabolic acidosis. The aim of this study was to compare, in a controlled volume-driven porcine model of hemorrhagic shock, the effects of three different crystalloid solutions on the hemodynamics and acid-base balance. METHODS: Controlled hemorrhagic shock (40 percent of the total blood volume was removed) was induced in 18 animals, which were then treated with normal saline (0.9 percent NaCl), Lactated Ringer's Solution or Plasma-Lyte pH 7.4, in a blinded fashion (n = 6 for each group). Using a predefined protocol, the animals received three times the volume of blood removed. RESULTS: The three different crystalloid infusions were equally capable of reversing the hemorrhage-induced low cardiac output and anuria. The Lactated Ringer's Solution and Plasma-Lyte pH 7.4 infusions resulted in an increased standard base excess and a decreased serum chloride level, whereas treatment with normal saline resulted in a decreased standard base excess and an increased serum chloride level. The Plasma-Lyte pH 7.4 infusions did not change the level of the unmeasured anions. CONCLUSION: Although the three tested crystalloid solutions were equally able to attenuate the hemodynamic and tissue perfusion disturbances, only the normal saline induced hyperchloremia and metabolic acidosis.

Magnesium chloride induced acidosis in malnutrition - abstract

Because their is a total body deficit of magnesium in malnutrition, magenesium salts are routinely prescribed in treatment. Several children were observed to develop severe hyperchloraemic acidosis after admission to the ward, and urine from recovering children was found to be highly acidic. This study tested the hypothesis that the acidosis was iatrogenically induced by the magnesium chloride supplement. Six malnourished and 5 recovering children were treated in the standard way except that they were given magnesium chloride (1 mmol/kg/d) for 4 days and then magnesium acetate for 4 days. The order of the salts was changed in alternate children. Jugular venous Astrup and timed urine collections were made at the end of each period. The malnourished children developed sytemic acidosis on the magnesium chloride supplement (pH 7.3 ñ 0.01 vs - #.6 ñ 1.1). Those children who were given the acetate salt first remained in acid-base equilibrium whereas those who were given the chloride first had not regained normal acid base status after 4 days on the acetate. On the chloride salt the urinary pH was lower (5.0 ñ 0.3 vs 6.5 ñ 0.3), the titratable acidity higher (1.5 ñ 0.2 vs 0.4 ñ 0.3 æEq/min) and the total acid (TA = ammonia - HCO3) output higher (5.5 ñ 0.8 vs 2.1 ñ 0.4 æEq/min), than on the acetate salt. The recovering children also developed a mild systemic acidosis on the chloride (Base excess - 5.5 ñ 0.9 vs 2.3 ñ 0.5) and excreted a highly acid urine, pH 4.8 ñ 0.1; on the acetate the urine was also acid pH 5.1 ñ 0.1. The total acidity output was 20.4 ñ 1.1 æEq/min on the chloride and 15.3 ñ 1.4æEq/min on the acetate. It is concluded that magnesium chloride is the cause of the iatrogenic systemic acidosis seen in our malnourished children. Whilst malnourished they excrete a maximally acid urine, however the total acid output is small and leads to a progressively positive hydrogen ion balance, which the child cannot correct within four days of ceasing the chloride load. This work was supported by the Wellcome Trust (AU)