Hypochloremic Alkalosis Medication

Replacement of electrolytes with chloride salts is the most important mode of therapy for hypochloremic alkalosis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in patients with Bartter syndrome. Hydrochloric acid (HCl) and carbonic anhydrase inhibitors may be used in some acute situations.

Class Summary

These agents are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance. They are also used to reestablish osmotic equilibrium of specific ions.

Potassium chloride

Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion or GI loss or because of low intake.

Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition. Potassium depletion sufficient to cause a 1 mEq/L drop in the serum potassium level requires a loss of approximately 100-200 mEq of potassium from the total body store.

Sodium chloride hypertonic, ophthalmic

For restoration of sodium ion in patients with restricted PO intake, especially hyponatremia states or salt-wasting syndromes. Administer sodium-containing parenteral solution with proper isotonicity.

Class Summary

These agents have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action is unknown, but NSAIDs may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also occur, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Indomethacin (Indocin)

Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.

Class Summary

The major pharmacologic action of acetazolamide is the noncompetitive inhibition of the enzyme carbonic anhydrase. Carbonic anhydrase is located at the luminal border of cells of the proximal tubule. Urine volume increases with enzyme inhibition (proximal tubule reabsorption of water is reduced by approximately one third), which promotes an alkaline pH. This results in a subsequent decrease in the excretion of titratable acid and ammonia. Increases in urinary excretion of bicarbonate and sodium lead to metabolic acidosis.

Acetazolamide (Diamox)

May be used in loop or thiazide diuretic-induced metabolic alkalosis, especially in edematous states.

Class Summary

Consequences of severe metabolic alkalosis include increased susceptibility to ventricular arrhythmia and a left shift of the oxyhemoglobin dissociation curve. HCl is particularly useful in patients with hepatic or renal impairment, which often precludes more standard treatments.

Hydrochloric acid

IV HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when NaCl or KCl cannot be administered because of volume overload or advanced renal failure. May also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity). Not commercially available and must be extemporaneously compounded from concentrated HCl solution. Dose is based on chloride deficit and base excess. Typically, concentration ranges from 0.1-0.15 N (ie, 100-150 mmol H⁺/L). Concentrations greater than 0.2 N may be associated with an increased risk of hemolysis. mEq HCl = body weight (kg) X 0.3 X base excess (mEq/L).

Class Summary

These agents are effective for treating diuretic-induced hyperuricemia and renal complications resulting in hyperuricemia.

Allopurinol (Zyloprim)

Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces synthesis of uric acid without disrupting biosynthesis of vital purines.