Bicarbonate

Metabolism of glucose, fats, and protein as energy source results in the production of carbon dioxide which acts as an acid in the body. Bicarbonate is part of a complex system of buffers to allow the body to maintain acid-base homeostatis. The ratio of the bicarbonate and carbon dioxide concentrations determines blood pH.

•	Metabolic acidosis. Once metabolic acidosis is diagnosed the next step is calculation of the anion gap. This helps to determine the cause of the acidosis. With a normal anion gap, the serum chloride is elevated, producing a hyperchloremic metabolic acidosis.

•	Conditions that promote hyperchloremia such as fistulas, diarrhea, or renal tubular acidosis.

•	States that cause lactic acidosis such as hypoxia, hypotension, sepsis, liver failure, or neoplasia.

•	Diabetic ketoacidosis and the sudden development of lactic acidosis.

•	Accumulation of inorganic and organic acids in renal failure.

Patients with metabolic acidosis display an arterial pH less than 7.35 and a serum bicarbonate less than 22 mEq/L .

Treat the underlying causes of excess fluid loss. For acute acidosis, bicarbonate 2 to 5 mEq/kg may be administered IV slowly over 4 to 8 hours. Stepwise correction of acidosis with frequent lab evaluation is preferred to avoid the complications of over-correction.

A TPN solution should not be utilized for bicarbonate administration due to the formation of insoluble calcium or magnesium salts. Reduce chloride in TPN by substituting acetate salts until the acidosis resolves and the serum pH, bicarbonate and chloride levels return to normal. Dialysis may be required for severe, poorly controlled metabolic acidosis.

•	Metabolic alkalosis. Metabolic alkalosis occurs as a result of improper anion balance in TPN. Because acetate is metabolized to bicarbonate, excessive acetate and inadequate chloride can produce metabolic alkalosis.

•	GI loss of acid and chloride due to vomiting, diarrhea, gastric suction, and fistulas.

Signs and symptoms include paresthesias, confusion, lightheadedness, tetany, and seizures.

Patients with metabolic alkalosis display an arterial pH greater than 7.45 and a serum bicarbonate greater than 28 mEq/L .

Treat underlying causes of excess chloride and acid loss, administer H-2 blockers to decrease acid loss. Avoid all lactate-containing IV solutions (e.g., Ringer's lactate) and administer IV saline.

Increase chloride intake by substituting chloride for acetate in the TPN. In patients with severe alkalosis it may be necessary to give acidifying compounds such as ammonium chloride or hydrochloric acid.