Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis

P. F. Moon, George Kramer

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Objective: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. Design: Blinded, randomized, control trial. Setting: Laboratory setting. Subjects: Sixteen healthy Yorkshire swine. Interventions: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic 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 given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. Measurements and Main Results: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant 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 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline/dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. Conclusions: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

Original languageEnglish (US)
Pages (from-to)323-331
Number of pages9
JournalCritical Care Medicine
Volume23
Issue number2
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

dextran - saline drug combination
Hemorrhagic Shock
Acidosis
Resuscitation
Shock
Swine
Acid-Base Equilibrium
Dextrans
Sodium Chloride
Cardiac Output
Electrolytes
Lactic Acid
Ions
Hypernatremia
Respiratory Acidosis
Lactic Acidosis
Proteins
Acids
Potassium Chloride
Hypokalemia

Keywords

  • acid-base equilibrium
  • anion gap
  • critical illness
  • electrolytes
  • fluid therapy
  • hyperchloremia
  • hypertonic saline solution
  • metabolic acidosis
  • pH
  • swine

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis. / Moon, P. F.; Kramer, George.

In: Critical Care Medicine, Vol. 23, No. 2, 1995, p. 323-331.

Research output: Contribution to journalArticle

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title = "Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis",
abstract = "Objective: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5{\%} sodium chloride/6{\%} dextran-70. Design: Blinded, randomized, control trial. Setting: Laboratory setting. Subjects: Sixteen healthy Yorkshire swine. Interventions: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic 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 given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5{\%} sodium chloride/6{\%} dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. Measurements and Main Results: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant 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 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline/dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. Conclusions: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.",
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T1 - Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis

AU - Moon, P. F.

AU - Kramer, George

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N2 - Objective: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. Design: Blinded, randomized, control trial. Setting: Laboratory setting. Subjects: Sixteen healthy Yorkshire swine. Interventions: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic 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 given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. Measurements and Main Results: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant 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 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline/dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. Conclusions: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

AB - Objective: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. Design: Blinded, randomized, control trial. Setting: Laboratory setting. Subjects: Sixteen healthy Yorkshire swine. Interventions: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic 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 given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. Measurements and Main Results: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant 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 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline/dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. Conclusions: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

KW - acid-base equilibrium

KW - anion gap

KW - critical illness

KW - electrolytes

KW - fluid therapy

KW - hyperchloremia

KW - hypertonic saline solution

KW - metabolic acidosis

KW - pH

KW - swine

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