Metabolic Alkalosis Medication
- Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
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.
Carbonic Anhydrase Inhibitors
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).
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.
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.
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 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).
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 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.
Angiotensin-Converting Enzyme Inhibitors
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 prevents 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 conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Potassium supplements may be used to correct metabolic alkalosis, which is often associated with hypokalemia.
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.
Fluid replacement is used in chloride-responsive alkalosis with volume depletion.
This volume expander solution is used to correct metabolic imbalances.
Corticosteroids are used in glucocorticoid-remediable hyperaldosteronism, metabolic alkalosis, and hypertension.
Dexamethasone suppresses cortisol production by inhibiting ACTH. It does not activate the mineralocorticoid receptor.
Nonsteroidal Anti-inflammatory Agents
NSAIDs may partially correct metabolic alkalosis in Bartter syndrome and Gitelman syndrome.
Ibuprofen inhibits inflammatory reactions and decreases prostaglandin synthesis.
Indomethacin is a rapidly absorbed NSAID. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. This agent inhibits prostaglandin synthesis.
Mehler PS, Walsh K. Electrolyte and acid-base abnormalities associated with purging behaviors. Int J Eat Disord. 2016 Mar. 49 (3):311-8. [Medline].
Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009 Mar. 84(3):261-7. [Medline]. [Full Text].
Tentori F, Karaboyas A, Robinson BM, Morgenstern H, Zhang J, Sen A, et al. Association of dialysate bicarbonate concentration with mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2013 Oct. 62(4):738-46. [Medline]. [Full Text].
Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol. 2008 Nov. 3(6):1861-8. [Medline].
Weise WJ, Serrano FA, Fought J, Gennari FJ. Acute electrolyte and acid-base disorders in patients with ileostomies: a case series. Am J Kidney Dis. 2008 Sep. 52(3):494-500. [Medline].
Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007 Jan. 2(1):162-74. [Medline]. [Full Text].
Stewart PA. How to understand acid-base: a quantitative acid-base primer for biology and medicine. [AcidBase.org]. Available at http://www.acidbase.org/index.php?show=sb. Accessed: Aug 10, 2009.
Kaplan LJ, Cheung NH, Maerz L, et al. A physicochemical approach to acid-base balance in critically ill trauma patients minimizes errors and reduces inappropriate plasma volume expansion. J Trauma. 2009 Apr. 66(4):1045-51. [Medline].
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].
Gennari FJ. Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport. Am J Kidney Dis. 2011 Oct. 58(4):626-36. [Medline].