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Metabolic Alkalosis Medication

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jul 26, 2016
 

Medication Summary

The choice of therapy in metabolic alkalosis varies with the underlying cause. Carbonic anhydrase inhibitors, hydrochloric acid (HCl), potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, potassium supplements, fluid replacements, and nonsteroidal anti-inflammatory drugs (NSAIDs) may be used in specific situations.[10]

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Carbonic Anhydrase Inhibitors

Class Summary

Diuretics may be used to treat severe metabolic alkalosis in edematous states (eg, from congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), or right heart failure).

Acetazolamide (Diamox)

 

This agent inhibits carbonic anhydrase, the enzyme that catalyzes the hydration of CO2 and dehydration of carbonic acid. Inhibition reduces reabsorption of NaHCO3 in the proximal tubule, leading to natriuresis, bicarbonate, diuresis, and a decreased serum bicarbonate level. As NaHCO3 delivery to the collecting duct increases, potassium secretion enhances, resulting in hypokalemia.

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Acids

Class Summary

Acidic IV solutions are used to treat severe metabolic alkalosis. Seek the advice of nephrologist in severe alkalosis when HCl therapy or dialysis is contemplated.

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. This approach may also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, in cases of cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity). HCl is available in preparations of 0.1 and 0.2 M, which contain 100 mmol H+/L and 200 mmol H+/L, respectively.

Ammonium chloride (NH4Cl)

 

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 tablets and a 26.75% parenteral formulation for intravenous use. The parenteral formulation contains 5 mEq/mL (267.5 mg/mL).

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Potassium-Sparing Diuretics

Class Summary

These agents may be used to correct potassium deficiency or fluid/electrolyte imbalance.

Triamterene (Dyrenium)

 

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 (Aldactone)

 

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 acid-base balance.

Amiloride

 

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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Angiotensin-Converting Enzyme Inhibitors

Class Summary

ACE inhibitors block conversion of angiotensin I to angiotensin II and prevent secretion of aldosterone from the adrenal cortex. These agents are indicated in metabolic alkalosis due to hyperaldosteronism.

Captopril

 

Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Enalapril (Vasotec)

 

A competitive inhibitor of ACE, enalapril reduces angiotensin II levels, decreasing aldosterone secretion.

Lisinopril (Prinivil, Zestril)

 

Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

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Potassium Supplements

Class Summary

Potassium supplements may be used to correct metabolic alkalosis, which is often associated with hypokalemia.

Potassium chloride (Epiklor, MicroK, Klor-Con)

 

Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function.

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Fluid Replacements

Class Summary

Fluid replacement is used in chloride-responsive alkalosis with volume depletion.

Sodium chloride hypertonic, ophthalmic

 

This volume expander solution is used to correct metabolic imbalances.

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Corticosteroids

Class Summary

Corticosteroids are used in glucocorticoid-remediable hyperaldosteronism, metabolic alkalosis, and hypertension.

Dexamethasone (Baycadron, Maxidex, Ozurdex)

 

Dexamethasone suppresses cortisol production by inhibiting ACTH. It does not activate the mineralocorticoid receptor.

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Nonsteroidal Anti-inflammatory Agents

Class Summary

NSAIDs may partially correct metabolic alkalosis in Bartter syndrome and Gitelman syndrome.

Ibuprofen (Motrin, Advil, NeoProfen)

 

Ibuprofen inhibits inflammatory reactions and decreases prostaglandin synthesis.

Indomethacin (Indocin)

 

Indomethacin is a rapidly absorbed NSAID. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. This agent inhibits prostaglandin synthesis.

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Contributor Information and Disclosures
Author

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Sameer Yaseen, MD Staff Nephrologist, Department of Internal Medicine, Division of Nephrology, Mercy Hospital of Des Moines

Sameer Yaseen, MD is a member of the following medical societies: Renal Physicians Association, American Society of Nephrology

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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  9. Fontana V, Santinelli S, Internullo M, Marinelli P, Sardo L, Alessandrini G, et al. Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients. Eur Rev Med Pharmacol Sci. 2016. 20 (1):37-43. [Medline].

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Algorithm for metabolic alkalosis.
 
 
 
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