A good review on acid-base disturbances: NEJM 2014; 371: 1434-45. This is good reading for those needing a refresher on any of the following:
- Metabolic acidosis: -high anion-gap vs. low anion-gap (Table 2)
- Metabolic alkalosis -mainly due to loss of gastric fluid and use of diuretics.
- Respiratory acidosis -associated with hypoventilation
- Respiratory alkalosis -associated with hyperventilation
Here’s a link: http://www.nejm.org/doi/full/10.1056/NEJMra1003327
A few useful pointers:
- Lactic acidosis –“roughly half the patients with serum lactate levels between 3.0 and 5.0 mmol per liter have an anion gap within the reference range.”
- Anion gap is affected by hypoalbuminemia. “For every decrement of 1 g per deciliter in the serum albumin concentration, the calculated anion gap should be increased by approximately 2.3 to 2.5 mmol per liter.”
- Low anion gap mainly due to loss of bicarbonate: GI conditions (like diarrhea or other GI fluid losses), renal losses of bicarbonate (RTAs, medicine-induced), decreased renal acid excretion, or other (eg. saline resuscitation, hyperalimentation (lysine, histidine, or argentine hydrochloride, cholestyramine, and other causes).
- High anion gap: overproduction of acid (lactic acidosis, ketoacidosis –DKA, alcoholic). Lactic acidosis can be due to D-lactic acidosis in short bowel syndrome or due to L-lactic acidosis (type A hypoxic, type B nonhypoxic -related to numerous medicines/intoxications/thiamine deficiency), advanced renal failure, impaired lactic clearance in liver failure, rhabdomyolysis, penicillin-derived antibiotics, and pyroglutamic acid.
Figure 1 provides an algorithm for sorting out acedemias including use of urinary anion gaps and Figure 2 does the same for alkalemias.