Bicarbonate (HCO₃) excess

Milk-alkali syndrome

₃ load; hypercalcemia lowers PTH, increasing HCO₃ reabsorption

NaHCO₃ loading

Occurs with overzealous loading or with loading in patients who have hypokalemia; serum becomes more alkalotic as H shifts back into cells

Posthypercapnic*

Persistent elevation of compensatory HCO₃ levels, often with volume, K, and Cl depletion

Postorganic acidosis

Conversion of lactic acid or ketoacid to HCO₃ worsened by HCO₃ therapy for acidosis

Contraction alkalosis*

Diuretics (all types)

Sweat loss in cystic fibrosis

NaCl loss concentrates a fixed amount of HCO₃ in a smaller total body volume

Gastrointestinal acid loss*

Congenital chloridorrhea

Fecal Cl loss and HCO₃ retention

Gastric acid loss due to vomiting or nasogastric suction

Loss of HCl and acid coupled with contraction alkalosis due to release of aldosterone and subsequent resorption of HCO₃

Villous adenoma

Probably secondary to K depletion

Renal acid loss

Bartter syndrome†

Rare congenital disease causing hyperaldosteronism and hypokalemic metabolic alkalosis that manifests in early childhood with renal salt wasting and volume depletion

Diuretics (thiazide and loop)‡

Multiple mechanisms: Secondary hyperaldosteronism due to volume depletion, Cl depletion, or contraction alkalosis; may be Cl-unresponsive because of concomitant K depletion

Gitelman syndrome†

Similar to Bartter syndrome

Characterized in addition by hypomagnesemia and hypocalciuria

Manifests in young adults

Hypokalemia and hypomagnesemia†

Stimulate K and Mg reabsorption and H excretion

Alkalosis unresponsive to NaCl and volume replacement until deficiencies corrected

Low K causing H to shift into cells, raising extracellular pH

Primary hyperaldosteronism†

Includes congenital adrenal hyperplasia

Secondary hyperaldosteronism†

Occurs with volume depletion, heart failure, cirrhosis with ascites, nephrotic syndrome, Cushing syndrome or disease, renal artery stenosis, or renin-secreting tumor

Use of glycyrrhizin-containing compounds† (eg, licorice, chewing tobacco, carbenoxolone, Lydia Pinkham’s vegetable compound)

Glycyrrhizin inhibition of enzymatic conversion of cortisol to less active metabolites

Other

Carbohydrate refeeding after starvation

Resolution of starvation ketosis or acidosis with improved cellular function

Laxative abuse*

Unclear mechanism

Some antibiotics (eg, carbenicillin, penicillin, ticarcillin)

Contain nonreabsorbable anion, which increases K and H excretion