Common Laboratory (LAB) Values - ABGs - GlobalRPH

1] Calculate the anion gap:

2] Based on the anion gap and patient history – review potential causes:

Normal anion gap (hyperchloremic) metabolic acidosis: Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap metabolic acidosis is also called hyperchloremic acidosis, because instead of reabsorbing HCO3- with Na, the kidney reabsorbs Cl-.    Many GI secretions are rich in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy (insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+.

Loss of HCO3 ions is accompanied by an increase in the serum Cl- concentration. The anion gap remains normal. Disease processes that can lead to normal anion gap (hyperchloremic) acidosis. Useful mnemonic (DURHAM): a) Diarrhea (HCO3- and water is lost). b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the gastrointestinal loss of HCO3-. c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate wastage of HCO3- and retention of Cl-. d) Hyperalimentation e) Acetazolamide f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal wastage of HCO3-.

Increased anion gap metabolic acidosisHigh anion gap acidosis: The most common causes of a high anion gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal failure causes anion gap acidosis by decreased acid excretion and decreased bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap.   Toxins may have acidic metabolites or trigger lactic acidosis.

In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The anions of these acids are not Cl- ions. The presence of these acid anions, which are not measured, will cause an increase in the anion gap. Useful mnemonic (MUD PILES):

Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver to formic acid. Uremia: In end-stage renal failure in which glomerular filtration rate falls below 10—20 ml/min, acids from protein metabolism are not excreted and accumulate in blood.

Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of beta-hydroxybutyric and acetoactic acids (ketoacids).

Paraldehyde poisoning.

Ischemia: causes lactic acidosis.

Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid, the end product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the Tricarboxylic Acid Cycle.  (Causes: hypoxia, ischemia, hypotension, sepsis).

Ethylene glycol poisoning:  Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the liver. Usually there is also a coexisting lactic acidosis.

Salicylate poisoning