Etiology of metabolic acidosis during saline resuscitation in endotoxemia.
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.
Kellum
J A
JA
Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh Medical Center, Pennsylvania 15213-2582, USA.
Bellomo
R
R
Kramer
D J
DJ
Pinsky
M R
MR
D000138:Acidosis / Q000097:blood / Q000209:etiology*; D000818:Animals; D001794:Blood Pressure; D002712:Chlorides / Q000097:blood; D004285:Dogs; D004573:Electrolytes / Q000097:blood; D019446:Endotoxemia / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D004731:Endotoxins; D004926:Escherichia coli; D008297:Male; D012151:Resuscitation; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000627:therapeutic use; D013997:Time Factors
D002712:Chlorides; D004573:Electrolytes; D004731:Endotoxins; D012965:Sodium Chloride; D012964:Sodium