Metabolic acidosis should be divided into an increased and normal AG acidosis. The term anion gap is misleading because the serum has no gap between total positive and negative ions; however, the unmeasured anions exceed the unmeasured cations.
No matter the etiology, acidosis can cause nausea and vomiting, abdominal pain, change in sensorium, and tachypnea, sometimes a Kussmaul respiratory pattern. Acidosis causes many negative physiologic effects that result in hypoxia. Patients may present with nonspecific complaints or shock.
Causes of metabolic acidosis can be divided into 2 main groups: (a) those associated with increased production of organic acids (Table 4-5); and (b) those associated with a loss of [HCO3−], failure to excrete [H+], or addition of [H+] (Table 4-6).
Causes of anion gap metabolic acidosis include renal failure, lactic acidosis, ketoacidosis, and toxins. A mnemonic to aid the recall of the causes of increased AG metabolic acidosis is: A MUD PILES: alcohol, methanol, uremia, DKA, paraldehyde, iron and isoniazid, lactic acidosis, ethylene glycol, salicylates, and starvation. Caution should be used when applying the A MUD PILES mnemonic because the presence of alcohol in the patient's blood does not rule out a more serious cause of acidosis. Iron and isoniazid exert their effects on the AG due to lactic acidosis. Causes of normal anion gap acidosis include GI or renal loss of [HCO3−]. A mnemonic that can aid the recall of normal AG metabolic acidosis is USED CARP:ureterostomy, small bowel fistulas, extra chloride, diarrhea, carbonic anhydrase inhibitors, adrenal insufficiency, renal tubular acidosis, and pancreatic fistula.
Indications for bicarbonate therapy are listed in Table 4-7. Give 0.5 mEq/kilogram bicarbonate for each mEq/L desired rise in [HCO3−]. The goal is to restore adequate buffer capacity ([HCO3−] > 8 mEq/dL) or achieve clinical improvement in shock or dysrhythmias. Seventy-five mEq of sodium bicarbonate in 500 mL D5W produces a nearly isotonic solution for infusion.