bicarbonate

Bicarbonate is filtered freely at the glomerulus and reabsorbed (~85-90%) in the proximal tubule via Na+/H+ exchanger (NHE3) and carbonic anhydrase-dependent mechanisms; additional reabsorption occurs in the thick ascending limb and distal nephron, where intercalated cells (type A) generate new bicarbonate via H+ secretion coupled to ammoniagenesis and titratable acid excretion. The Henderson-Hasselbalch equation (pH = 6.1 + log[HCO3-]/(0.03×PCO2)) governs the relationship between bicarbonate, CO2, and pH, forming the basis for interpreting acid-base disorders. Low serum bicarbonate suggests metabolic acidosis (either from HCO3- loss—diarrhea, RTA—or consumption by buffering excess acid—DKA, lactic acidosis, uremia; distinguished via anion gap) or respiratory alkalosis compensation. High bicarbonate suggests metabolic alkalosis (vomiting, diuretics, hyperaldosteronism) or renal compensation for chronic respiratory acidosis (COPD). Winter's formula predicts expected respiratory compensation in metabolic acidosis. Bicarbonate is also used therapeutically: IV sodium bicarbonate treats severe metabolic acidosis, hyperkalemia (shifts K+ intracellularly), TCA overdose (widens QRS, alkalinizes to reduce Na channel blockade), and urine alkalinization in salicylate toxicity or rhabdomyolysis to enhance excretion. Renal tubular acidosis types (I, II, IV) are classic board topics testing bicarbonate handling defects. Bicarbonate also plays a key role in the chloride shift (Hamburger phenomenon) in RBCs during CO2 transport from tissues to lungs.