Overview
Clinical Meaning
Metabolic acidosis is characterized by decreased serum bicarbonate (<22 mEq/L) and decreased pH (<7.35), with respiratory compensation (hyperventilation — Kussmaul breathing).
NCLEX-RN
NCLEX-RN
Metabolic acidosis is characterized by decreased serum bicarbonate (<22 mEq/L) and decreased pH (<7.35), with respiratory compensation (hyperventilation — Kussmaul breathing). It is classified by the anion gap (AG = Na - [Cl + HCO3], normal 8-12): elevated anion gap metabolic acidosis (AGMA) indicates accumulation of unmeasured acids, while normal anion gap (non-gap or hyperchloremic) metabolic acidosis indicates bicarbonate loss or impaired acid excretion. AGMA causes are remembered by MUDPILES: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. Normal AG causes include diarrhea (GI bicarbonate loss), renal tubular acidosis, carbonic anhydrase inhibitors, and IV normal saline (dilutional). Severe metabolic acidosis (pH <7.1) is a medical emergency: cardiac contractility decreases, arrhythmia threshold lowers, vasodilation occurs, catecholamine resistance develops, and enzyme systems fail. The RN must monitor for Kussmaul breathing (deep, rapid respirations — the body's attempt to blow off CO2 and compensate for the metabolic acidosis), assess for the underlying cause, and understand that bicarbonate administration is controversial and reserved for pH <6.9-7.1 in most guidelines.
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