Pediatric Metabolic Alkalosis Medication
- Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD more...
Metabolic alkalosis that results from chloride depletion and volume contraction can often be corrected with volume replacement. Persistent severe metabolic alkalosis may require more specific therapy directed at moderating the alkalemia.
These solutions are the recommended therapeutic agents for rapid correction of severe metabolic alkalosis, especially metabolic alkalosis due to gastric losses of chloride.
Hydrochloric acid (HCl)
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. It may also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity).
The amount of HCl required to correct metabolic alkalosis is determined by estimating the amount of pH deficit, the volume, and the infusion rate of HCl solution. The typical HCl preparation contains 0.1 N solution (ie, 100 mmol H+/L [mEq/L]) in D5W or 0.9% NaCl).
Ammonium chloride is administered to correct severe metabolic alkalosis related to chloride deficiency. NH4Cl is converted to ammonia and HCl by the liver. By releasing HCl, NH4Cl may help correct metabolic alkalosis.
This agent is available as 500-mg tabs and 26.75% parenteral formulation for IV use. The parenteral formulation contains 5 mEq/mL (267.5 mg/mL).
Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, and maintenance of intracellular tonicity, skeletal and smooth muscles, and normal renal function. Metabolic alkalosis is often associated with hypokalemia.
Angiotensin-Converting Enzyme Inhibitors
ACE inhibitors block the conversion of angiotensin I to angiotensin II and prevent the secretion of aldosterone from the adrenal cortex. These agents are indicated in metabolic alkalosis due to hyperaldosteronism.
Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
A competitive inhibitor of ACE, enalapril reduces angiotensin II levels, decreasing aldosterone secretion.
Lisinopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Carbonic Anhydrase Inhibitors
These agents may be used to treat chloride-resistant metabolic alkalosis.
Acetazolamide is a carbonic anhydrase inhibitor that blocks HCO3 reabsorption in the proximal renal tubules. It causes increased renal excretion of sodium vs chloride, causing a net increase in serum chloride. Acetazolamide is also a diuretic and, therefore, may help decrease extracellular fluid (ECF) volume that frequently accompanies chloride-resistant metabolic alkalosis.
These agents may be used to correct potassium deficiency or fluid/electrolyte imbalance.
Triamterene interferes with potassium/sodium exchange (active transport) in the distal tubule, cortical collecting tubule, and collecting duct by inhibiting sodium/potassium adenosine triphosphatase (ATPase). This agent decreases calcium excretion and increases magnesium loss.
Spironolactone is an aldosterone antagonist that competitively inhibits binding to the aldosterone receptor. It competes for receptor sites in distal renal tubules and increases water excretion while retaining potassium and hydrogen ions needed to restore the acid-base balance.
Amiloride is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known potassium-conserving (antikaliuretic) or diuretic agents. It is an antikaliuretic drug, which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.
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