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Etiology of metabolic acidosis during saline resuscitation in endotoxemia

Kellum, JA and Bellomo, R and Kramer, DJ and Pinsky, MR (1998) Etiology of metabolic acidosis during saline resuscitation in endotoxemia. Shock, 9 (5). 364 - 368. ISSN 1073-2322

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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.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Kellum, JAkellum@pitt.eduKELLUM0000-0003-1995-2653
Bellomo, R
Kramer, DJ
Pinsky, MRpinsky@pitt.eduPINSKY0000-0001-6166-700X
Date: 1 January 1998
Date Type: Publication
Journal or Publication Title: Shock
Volume: 9
Number: 5
Page Range: 364 - 368
DOI or Unique Handle: 10.1097/00024382-199805000-00009
Schools and Programs: School of Medicine > Critical Care Medicine
Refereed: Yes
ISSN: 1073-2322
PubMed ID: 9617887
Date Deposited: 13 Mar 2012 15:50
Last Modified: 22 Jun 2021 14:55


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