Etiology of metabolic acidosis during saline resuscitation in endotoxemia

Shock. 1998 May;9(5):364-8. doi: 10.1097/00024382-199805000-00009.


We sought to understand the mechanism of metabolic acidosis that results in acute resuscitated endotoxic shock. In six pentobarbital-anesthetized dogs, shock was induced by Escherichia coli endotoxin infusion (1 mg/kg) and was treated with saline infusion to maintain mean arterial pressure > 80 mmHg. Blood gases and strong ions were measured during control conditions and at 15, 45, 90, and 180 min after endotoxin infusion. The mean saline requirement was 1833+/-523 mL over a 3 h period. The total acid load from each source was calculated using the standard base deficit. The mean arterial pH decreased from 7.32 to 7.11 (p < .01); pCO2 and lactate were unchanged. Saline accounted for 42% of the total acid load. However, 52% of the total acid load was unexplained. Although serum Na+ did not change, serum Cl-increased (127.7+/-5.1 mmol/L vs. 137.0+/-6.1 mmol/L; p=.016). We conclude that saline resuscitation alone accounts for more than one-third of the acidosis seen in this canine model of acute endotoxemia, whereas lactate accounts for less than 10%. A large amount of the acid load can be attributed to differential Na+ and Cl- shifts from extravascular to vascular spaces.

MeSH terms

  • Acidosis / blood
  • Acidosis / etiology*
  • Animals
  • Blood Pressure
  • Chlorides / blood
  • Dogs
  • Electrolytes / blood
  • Endotoxemia / complications
  • Endotoxemia / physiopathology*
  • Endotoxemia / therapy
  • Endotoxins
  • Escherichia coli
  • Male
  • Resuscitation*
  • Sodium / blood
  • Sodium Chloride / therapeutic use
  • Time Factors


  • Chlorides
  • Electrolytes
  • Endotoxins
  • Sodium Chloride
  • Sodium