eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders
Metabolic Alkalosis: Treatment & Medication
Updated: Aug 18, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
The management of metabolic alkalosis depends primarily on the underlying etiology and on the volume status of the patient. In the case of vomiting, administer antiemetics, if possible. If continuous gastric suction is necessary, gastric acid secretion can be reduced with H2-blockers or more efficiently with proton-pump inhibitors. In patients who are on thiazide or loop diuretics, the dose can be reduced or the drug can be stopped if appropriate. Alternatively, potassium-sparing diuretics or acetazolamide can be added.
- Chloride-responsive alkalosis (general)
- If chloride-responsive alkalosis occurs with volume depletion, treat the alkalosis with an intravenous infusion of isotonic sodium chloride solution. Because this type of alkalosis is usually associated with hypokalemia, also use potassium chloride to correct the hypokalemia.
- If chloride-responsive alkalosis occurs in the setting of edematous states (eg, congestive heart failure [CHF]), use potassium chloride to correct the alkalosis instead of sodium chloride to avoid volume overload. If diuresis is needed, a carbonic anhydrase inhibitor (eg, acetazolamide) or a potassium-sparing diuretic (eg, spironolactone, amiloride, triamterene) can be used to correct the alkalosis.
- Chloride-resistant metabolic alkalosis (specific) - Depends on underlying cause
- Primary hyperaldosteronism: Metabolic alkalosis is corrected with the aldosterone antagonist spironolactone or with other potassium-sparing diuretics (eg, amiloride, triamterene). If the cause of primary hyperaldosteronism is an adrenal adenoma or carcinoma, surgical removal of the tumor should correct the alkalosis. In glucocorticoid-remediable hyperaldosteronism, metabolic alkalosis and hypertension are responsive to dexamethasone.
- Cushing syndrome: Potassium-sparing diuretics should correct the alkalosis until surgical therapy. Definitive therapy includes transsphenoidal microresection of ACTH-producing pituitary adenomas and adrenalectomy for adrenal tumors.
- Syndrome of AME: Metabolic alkalosis may be treated with potassium-sparing diuretics. On the other hand, dexamethasone may be used to suppress cortisol production by inhibiting ACTH. Unlike cortisol and some synthetic glucocorticoids, dexamethasone does not activate the mineralocorticoid receptor.
- Licorice ingestion: Discontinuation of licorice ingestion corrects the alkalosis; however, because full recovery of the enzyme 11B-HSD may occur as long as 2 weeks following long-term licorice use, potassium-sparing diuretics can be used during this interval.
- Bartter syndrome and Gitelman syndrome: Metabolic alkalosis can be corrected partially with potassium supplementation, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs, or ACE inhibitors.
- Liddle syndrome: Metabolic alkalosis can be treated with amiloride or triamterene but not with spironolactone. Both amiloride and triamterene inhibit the apical sodium ion channel in the collecting duct. Spironolactone, which is an MR antagonist working upstream of the defective sodium ion channel, does not correct the alkalosis or the hypertension.
- All metabolic alkalosis (specialized)
- Hydrochloric acid: Intravenous HCl is indicated in severe metabolic alkalosis (pH >7.55) or when sodium or potassium chloride cannot be administered because of volume overload or advanced renal failure. HCl may also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmias, hepatic encephalopathy, digoxin cardiotoxicity). Seek the advice of a nephrologist when severe alkalosis is present and HCl therapy or dialysis is contemplated.
- Dialysis: Both peritoneal dialysis and hemodialysis can be used with certain modifications of the dialysate to correct metabolic alkalosis. The main indication of dialysis in metabolic alkalosis is in patients with advanced renal failure, who usually have volume overload and are resistant to acetazolamide. With hemodialysis, metabolic alkalosis may be corrected by using a low-bicarbonate dialysate (bicarbonate can be as low as 18 mmol/L). Otherwise, acetate-free biofiltration (buffer-free dialysate), in which bicarbonate is not present in the dialysate but is infused separately as needed, may be used. In peritoneal dialysis, dialysis can be performed using isotonic sodium chloride solution as the dialysate.
Consultations
Seek the advice of a nephrologist when severe alkalosis is present and HCl therapy or dialysis is contemplated.
Medication
Carbonic anhydrase inhibitors and HCl are used to treat metabolic alkalosis.7
Carbonic anhydrase inhibitors
Diuretics may be used to treat severe metabolic alkalosis in edematous states (eg, CHF, COPD, right heart failure).
Acetazolamide (Diamox)
Inhibits carbonic anhydrase, the enzyme that catalyzes the hydration of CO2 and dehydration of carbonic acid. Inhibition reduces reabsorption of NaHCO3 in proximal tubule, leading to natriuresis, bicarbonate, diuresis, and a decreased serum bicarbonate. As NaHCO3 delivery to the collecting duct increases, potassium secretion enhances, resulting in hypokalemia.
Adult
250-500 mg PO q6h
5 mg/kg IV qd
Pediatric
Not established
Can decrease lithium levels; alters excretion of certain drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by causing alkalinization of the urine; increases cyclosporine toxicity; may increase salicylate toxicity
Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction; volume depletion; severe hypokalemia
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Concomitant administration with aspirin has been reported to cause anorexia, tachypnea, lethargy, coma, and death; caution in COPD or other lung disease associated with CO2 retention (may lead to more CO2 retention and hypoxemia); correct hypokalemia before beginning therapy
Acids
IV acidic 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. Also may be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity).
Preparations: 0.1-0.2 M, which contain 100 mmol H+/L and 200 mmol H+/L, respectively.
Adult
0.5 X lean body weight (kg) X desired decrement in plasma HCO3 - (mEq/L) IV infusion; not to exceed 0.2 mmol/kg/h; 15-20 mEq/h
Pediatric
Administer as in adults
Not established
Administration via a peripheral intravenous line
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Administer through central line in ICU; monitor ABGs and serum electrolytes
Potassium-sparing diuretics
May be used to correct potassium deficiency or fluid/electrolyte imbalance.
Triamterene (Dyrenium)
Interferes with potassium/sodium exchange (active transport) in distal tubule, cortical collecting tubule, and collecting duct by inhibiting sodium/potassium ATPase. Decreases calcium excretion and increases magnesium loss.
Adult
100 mg PO bid
Pediatric
Not established
Concurrent use with amiloride, spironolactone, or ACE inhibitors increases risk of hyperkalemia; amantadine plasma levels may increase and urinary excretion may decrease; cimetidine increases bioavailability and decreases clearance; avoid concurrent use with indomethacin because of increased risk of renal failure
Documented hypersensitivity; hyperkalemia; diabetes; renal impairment; concurrent use of potassium supplements, amiloride, or spironolactone unless documented evidence of unresponsiveness
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in severe hepatic encephalopathy, diabetes, renal dysfunction, and history of renal stones; monitor BUN and serum potassium to check kidney function; can cause mild nitrogen retention (reversible upon withdrawal); photosensitization and megaloblastic anemia may occur
Spironolactone (Aldactone)
Aldosterone antagonist that competitively inhibits binding to aldosterone receptor. Competes for receptor sites in distal renal tubules and increases water excretion while retaining potassium and hydrogen ions needed to restore acid-base balance.
Adult
50-100 mg PO q6h
Pediatric
Not established
May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase risk of hyperkalemia
Documented hypersensitivity; anuria; renal failure; hyperkalemia
Pregnancy
D - Unsafe in pregnancy
Precautions
Caution in renal and hepatic impairment
Amiloride (Midamor)
A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.
Adult
5-20 mg PO qd
Pediatric
Not established
NSAIDs decrease effects; ACE inhibitors, potassium preparations, and potassium-sparing diuretics increase risk of hyperkalemia; increased toxicity of lithium and amantadine
Documented hypersensitivity; hyperkalemia; potassium supplementation; impaired renal function; concurrent use of potassium-sparing diuretics; diabetic nephropathy
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Monitor electrolytes closely with evidence of renal function impairment, ie, BUN >30 mg/100 mL or serum creatinine levels >1.5 mg/100 mL; caution in severe hepatic encephalopathy, diabetes, and potassium retention associated with use of an antikaliuretic agent (accentuated in presence of renal impairment and may result in rapid development of hyperkalemia); monitor BUN and serum potassium; mild hyperkalemia is usually not associated with abnormal findings on ECG; can cause mild nitrogen retention, reversible upon withdrawal; photosensitization
Angiotensin-converting enzyme inhibitors
Block conversion of angiotensin I to angiotensin II and prevent secretion of aldosterone from the adrenal cortex.
Captopril (Capoten)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Adult
6.25-50 mg PO tid
Pediatric
Not established
NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when administered concurrently with diuretics
Documented hypersensitivity; renal impairment
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Enalapril (Vasotec)
Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.
Adult
2.5-20 mg PO qd
Pediatric
Not established
May increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; diuretics may enhance hypotensive effects; NSAIDs may reduce hypotensive effects
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Lisinopril (Prinivil, Zestril)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Adult
5-20 mg PO qd
Pediatric
Not established
May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; diuretics increase hypotensive effects; NSAIDs may reduce hypotensive effects
Documented hypersensitivity
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Potassium supplements
May be used to correct metabolic alkalosis.
Potassium chloride (K-Dur, Gen-K, Klor-Con)
Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function.
Adult
20-120 mEq PO qd
Pediatric
Not established
Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin
Documented hypersensitivity; hyperkalemia; renal failure; oliguria; azotemia; crush syndrome; anuria; adrenocortical insufficiency; potassium retention
Pregnancy
A - Safe in pregnancy
Precautions
Do not infuse rapidly; high plasma concentrations may cause death from cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor replacement therapy whenever possible by continuous or serial ECG; when a concentration >40 mEq/L is infused, local pain and phlebitis may follow
Fluid replacements
Used in chloride-responsive alkalosis with volume depletion.
Sodium chloride (Adsorbonac, SalineX)
Volume expander solution used to correct metabolic imbalances.
Adult
Volume status dependent
Pediatric
Volume status dependent
May decrease levels of lithium when administered concurrently
Poor renal function; inadequate urine output; pulmonary edema (the added fluid promotes more edema); hypernatremia; hypertonic uterus
Pregnancy
A - Safe in pregnancy
Precautions
Interstitial edema; edema in the brain or lungs is potentially fatal; volume overload may occur in poor renal function; caution in CHF, hypertension, liver cirrhosis, and sodium toxicity
Corticosteroids
Used in glucocorticoid-remediable hyperaldosteronism, metabolic alkalosis, and hypertension.
Dexamethasone (Decadron, Dexone)
Used to suppress cortisol production by inhibiting ACTH. Does not activate mineralocorticoid receptor.
Adult
0.5-4 mg PO bid
Pediatric
Not established
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Nonsteroidal anti-inflammatory agents
May partially correct metabolic alkalosis in Bartter syndrome and Gitelman syndrome.
Ibuprofen (Motrin, Advil)
Inhibits inflammatory reactions and decreases prostaglandin synthesis.
Adult
400-600 mg PO q6h
Pediatric
5-10 mg/kg PO q6h
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Pregnancy category D in third trimester; caution in CHF, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Indomethacin (Indocin, Indochron E-R)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.
Adult
25-50 mg PO q8h
Pediatric
1-3 mg/kg/d PO divided tid
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding; renal insufficiency
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
Pregnancy category D in third trimester; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs)
More on Metabolic Alkalosis |
| Overview: Metabolic Alkalosis |
| Differential Diagnoses & Workup: Metabolic Alkalosis |
 Treatment & Medication: Metabolic Alkalosis |
| Follow-up: Metabolic Alkalosis |
| Multimedia: Metabolic Alkalosis |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. Jan 2007;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. Apr 2009;66(4):1045-51. [Medline].
Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol. Nov 2008;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. Sep 2008;52(3):494-500. [Medline].
Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. Mar 2009;84(3):261-7. [Medline].
Banieghbal B. Rapid correction of metabolic alkalosis in hypertrophic pyloric stenosis with intravenous cimetidine: preliminary results. Pediatr Surg Int. Mar 2009;25(3):269-71. [Medline].
Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. Jan 8 1998;338(2):107-11. [Medline].
Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and surgical patients. Southern Medical Journal. 1987;80:729- 33. [Medline].
Babior BM. Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances. American Journal of Medicine. 1966;41:615- 21. [Medline].
Cruz DN, Perazella MA. Hypertension and hypokalemia: unusual syndromes. Conn Med. Feb 1997;61(2):67-75. [Medline].
DuBose TD Jr. Metabolic alkalosis. In: Brenner and Rector's The Kidney. 6th ed. Philadelphia: WB Saunders; 2000:971-997.
Galla JH. Metabolic Alkalosis. Journal of the American Society of Nephrology. 2000;11:369- 75. [Medline].
Geller DS, Farhi A, Pinkerton N. Activating mineralocorticoid receptor mutation in hypertension exacerbated by pregnancy. Science. Jul 7 2000;289(5476):119-23. [Medline].
Hixson R, Christmas D. Use of omeprazole in life-threatening metabolic alkalosis. Intensive Care Med. Oct 1999;25(10):1201. [Medline].
Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Critical Care Medicine. 1980;8:725- 8. [Medline].
Kaplan NM. Primary aldosteronism. In: Clinical Hypertension. 7th ed. Philadelphia: Williams & Wilkins; 1998:365-79.
Kaplan NM. Hypertension induced by cortisol or deoxycorticosterone. In: Clinical Hypertension. 7th ed. Philadelphia: Williams & Wilkins; 1998:383-392.
Kelleher SP, Schulman G. Severe metabolic alkalosis complicating regional citrate hemodialysis. Am J Kidney Dis. Mar 1987;9(3):235-6. [Medline].
Koeppen BM, Stanton BA. Regulation of acid-base balance. In: Vander AJ, ed. Renal Physiology. 2nd ed. New York: McGraw-Hill; 1997:135-55.
Kunau RT, et al. Acid-base balance. In: MKSAP: Nephrology and Hypertension Book. 1998. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 252-69.
Leblanc M, Farah A. Severe metabolic alkalosis corrected by hemodialysis. Clin Nephrol. Jul 1997;48(1):65. [Medline].
Mauri S, Pedroli G, Rudeberg A. Acute metabolic alkalosis in cystic fibrosis: prospective study and review of the literature. Miner Electrolyte Metab. 1997;23(1):33-7. [Medline].
Mazur JE, Devlin JW, Peters MJ. Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: a randomized, double-blind trial. Crit Care Med. Jul 1999;27(7):1257-61. [Medline].
McAuliffe JJ, Lind LJ, Leith DE. Hypoproteinemic alkalosis. Am J Med. Jul 1986;81(1):86-90. [Medline].
Online Mendelian Inheritance in Man (OMIM). McKusick-Nathans Institute for Genetic Medicine, Johns Hopkins University (Baltimore, MD) and National Center for Biotechnology Information, National Library of Medicine (Bethesda, MD). OMIM. 2000. [Full Text].
Palmer BF, Alpern RJ. Metabolic alkalosis. J Am Soc Nephrol. Sep 1997;8(9):1462-9. [Medline].
Rose BD. Metabolic alkalosis. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York: McGraw-Hill; 1994:515-35.
Rose BD. Acid-base physiology and regulation of acid-base balance. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York: McGraw-Hill; 1994:274-339.
Rose BD. Metabolic alkalosis. UpToDate. Available at www.uptodate.com.
Scheinman SJ, Guay-Woodford LM, Thakker RV. Genetic disorders of renal electrolyte transport. N Engl J Med. Apr 15 1999;340(15):1177-87. [Medline].
Seldin DW, Rector FC. Symposium on acid-base homeostasis. The generation and maintenance of metabolic alkalosis. Kidney Int. May 1972;1(5):306-21. [Medline].
Stewart PM. Cortisol as a mineralocorticoid in human disease. J Steroid Biochem Mol Biol. Apr-Jun 1999;69(1-6):403-8. [Medline].
Stewart PM, Walker BR, Holder G. 11 beta-Hydroxysteroid dehydrogenase activity in Cushing''s syndrome: explaining the mineralocorticoid excess state of the ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab. Dec 1995;80(12):3617-20. [Medline].
Toto RD, Alpern RJ. Metabolic acid-base disorders. In: Kokko JP, Tannen RL, eds. Fluids and Electrolytes. 3rd ed. Philadelphia: WB Saunders; 1996:201-56.
Zucchelli P, Santoro A. Correction of acid-base balance by dialysis. Kidney Int Suppl. Jun 1993;41:S179-83. [Medline].
Further Reading
Related eMedicine topics:
Alkalosis, Metabolic
Bartter Syndrome [Nephrology]
Bartter Syndrome [Pediatrics: General Medicine]
Hyperchloremic Acidosis
Hypertrophic Pyloric Stenosis
Hypertrophic Pyloric Stenosis, Surgical Treatment
Metabolic Acidosis [Emergency Medicine]
Metabolic Acidosis [Nephrology]
Respiratory Alkalosis
Clinical guidelines:
Evidence based clinical practice guideline hypertrophic pyloric stenosis. Cincinnati Children's Hospital Medical Center - Hospital/Medical Center. 2001 Aug 8 (revised 2007 Nov 4). 17 pages. NGC:006224
Clinical trials:
Acetazolamide for Respiratory Failure in Combination With Metabolic Alkalosis
Treatment of Metabolic Alkalosis in Acute Exacerbations of Cystic Fibrosis
Keywords
metabolic alkalosis, alkalosis, metabolic acidosis, anion gap, respiratory alkalosis, respiratory metabolic alkalosis, bicarbonate, metabolic anion gap, contraction alkalosis, chloride-resistant alkalosis, chloride-responsive alkalosis
