Metabolic acidosis is characterized by a primary decrease in serum bicarbonate (HCO3- <22 mmol/L) with a compensatory decrease in PaCO2 (respiratory compensation - Kussmaul breathing). It is classified by the anion gap (AG = Na+ - (Cl- + HCO3-), normal 8–12 mmol/L). Anion gap metabolic acidosis (AGMA) results from accumulation of unmeasured acids: the excess acid is buffered by bicarbonate (consuming HCO3-) while an unmeasured anion accumulates in the serum, widening the gap. The mnemonic MUDPILES identifies causes: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol/Paraldehyde, Isoniazid/Iron, Lactic acidosis (shock, sepsis, liver failure), Ethylene glycol, Salicylates. Non-anion gap metabolic acidosis (NAGMA, also called hyperchloremic metabolic acidosis) results from direct loss of bicarbonate (diarrhea - most common cause, RTA type 2) or failure to excrete hydrogen ions (RTA type 1, type 4). In NAGMA, chloride rises to replace lost bicarbonate, maintaining electrical neutrality and a normal anion gap. The kidneys compensate by excreting more acid and generating new bicarbonate, while the lungs compensate by hyperventilation (blowing off CO2). Kussmaul breathing (deep, rapid respirations) is the respiratory compensation for metabolic acidosis, particularly prominent in...