Interpretation of Bicarbonate Results

Decreased Bicarbonate
  • False decrease
    Decreases in bicarbonate occurs in aged samples. This is usually due to lactate production by cells, with buffering of bicarbonate. Overdilution with heparin and prolonged venous stasis will also decrease bicarbonate.

  • Metabolic acidosis
    Unless there is clear evidence of a respiratory disorder that would cause accumulation of CO2, low bicarbonate is presumptive evidence of metabolic acidosis. Diseases that cause loss or titration of HCO3 must then be considered. Evaluation of the anion gap helps distinguish between these causes, although both may be occurring concurrently resulting in a mixed acid-base disorder. Metabolic acidosis is the most common acid-base disorder encountered in veterinary practice.

    1) Loss of bicarbonate - normal anion gap hyperchloremic metabolic acidosis
    Bicarbonate is lost through the gastrointestinal tract (vomiting of biliary or pancreatic fluids, diarrhea, saliva, sequestration of bicarbonate within the gastrointestinal tract) or kidneys (renal tubular acidosis, Addison's disease). In cattle, saliva is high in bicarbonate, so loss of saliva through inability to swallow can result in a metabolic acidosis.
    In these conditions, water and sodium are lost concurrently, hence hypovolemia ensues. As a response to hypovolemia, the kidney absorbs sodium and water. Sodium is absorbed with chloride, which then increases in blood, resulting in hyperchloremia with a normal anion gap.

    2) Titration of bicarbonate - high anion gap metabolic acidosis
    Titration of bicarbonate by acids that lack chloride as the anion (unmeasured anion) will increase the anion gap. This is by far the most common cause of metabolic acidosis in animals. Acids that are unmeasured anions include lactate, organic acids (sulfates, phosphates and citrates), ketones (diabetic ketoacidosis), and ethelyene glycol and its metabolites. In these conditions, bicarbonate is consumed in buffering the organic acid, leaving the anion of the acid in its place (thus increasing the anion gap).
    Lactic acidosis usually results from decreased tissue perfusion (anaerobic glycolysis increases lactate production), e.g. hypovolemia, hypoxia. Lactic acidosis also results from grain overload in cattle. Renal failure will result in a high anion gap due to retained organic acids normally filtered by the kidney. Ketones (acetoacetic acid, beta-hydroxybutyrate) accumulate in unregulated diabetic patients. The lack of insulin leads to increased lipolysis of adipose tissue with enhanced fatty acid presentation to the liver. These fatty acids are used for energy, incorporated into lipoproteins (VLDL) or shunted into ketone production. Horses do not develop ketosis due to poorly developed ketone pathways. In contrast, llamas can become ketotic when energy-deprived (severe stress in pregnancy) resulting in ketosis. Dogs and cats with antifreeze (ethylene glycol) poisoning have very high anion gaps caused by metabolites of ethylene glycol.
Increased Bicarbonate

This usually indicates a metabolic alkalosis and is associated with hypochloremia. Artifactual causes for an increased HCO3 are quite rare. Metabolic alkalosis develops when gastric or abomasal secretions are lost in vomiting or are sequestered. In this situation, both H+ and Cl- are lost. Gastric cells continue to produce HCl, a reaction that generates sodium bicarbonate and the HCO3 is retained. The net effect of acid (H+) loss and base (HCO3) gain is a rise in blood pH. The hallmarks of metabolic alkalosis are increased bicarbonate and hypochloremia, usually with volume depletion, hypokalemia (K+ also is lost in gastric secretions) and a paradoxic aciduria.
In small animals, vomiting due to pyloric obstruction, e.g. foreign body or some cases of gastric dilatation-volvulus, causes metabolic alkalosis. In contrast to gastric secretions, duodenal and pancreatic secretions are very rich in HCO3. Therefore, if small intestinal contents as well as gastric secretions are lost in vomiting, which is more often the case, then metabolic acidosis, rather than alkalosis, develops.
In horses, hypochloremia, hypokalemia, and metabolic alkalosis can develop when overexerted, through loss of water and chloride-rich electrolytes in sweating.
Metabolic alkalosis is the most frequent acid-base abnormality in adult cattle and is usually due to either a displaced abomasum or abomasal atony (which can occur with vagus indigestion or in sick cattle with other disorders that do not primarily affect the gastrointestinal tract via unknown mechanisms). Any other disorder, in which abomasal outflow is impaired or obstructed. e.g. abomasal adhesions, abomasal inflammation, pressure on the abomasum from a fetus in advanced pregnancy, can result in sequestration of HCl and metabolic alkalosis.

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