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==Overview==
==Overview==
'''Metabolic alkalosis''' is an elevation of the pH in the bloodstream which results from decreased [[hydrogen]] ion concentration leading to increased [[bicarbonate]] and [[carbon dioxide]] concentrations, or alternatively a direct result of increased [[bicarbonate]] concentrations.
'''Metabolic alkalosis''' is an elevation of the pH in the bloodstream which results from decreased [[hydrogen]] ion concentration leading to increased [[bicarbonate]] and [[carbon dioxide]] concentrations, or alternatively a direct result of increased [[bicarbonate]] concentrations.
==Pathophysiology==
===Loss of hydrogen ions===
====GI loss====
* [[Vomiting]] (excretion of hydrogen ions and the retention of bicarbonate)
* [[Nasogastric tube]] suction
====Renal====
* Over-[[diuresis]]
* [[Hyperaldosteronism]] causing retention of sodium followed with compensatory excretion of hydrogen
* Administration of non-resorbable anions such as, [[penicillin]], [[carbenicillin]], which complexs with positively-charged hydrogen ions in the [[renal tubules]].
===Increase in the serum bicarbonate===
* Ingestion of [[sodium bicarbonate]], baking soda, citrate, lactate, or acetate.
===Shift of hydrogen ions into intracellular space===
* Seen in [[hypokalemia]].  Due to a low extracellular potassium concentration, potassium shifts out of the cells, and in order to maintain electrical neutrality, hydrogen shifts into the cells, leaving behind bicarbonate.
===Contraction alkalosis===
* This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use.  Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.
===Compensation for Metabolic Alkalosis===
* The body attempts to compensate for the increase in pH by retaining [[carbon dioxide]] (CO<sub>2</sub>) through [[hypoventilation]] ([[respiratory compensation]]). CO<sub>2</sub> combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.
* The pCO2 rises 0.5 - 1 for every 1 unit increase in serum HCO3 from a baseline of 24. 
* The maximum pCO2 in compensation is 55-60.
* [[Renal compensation]] for metabolic alkalosis consists of increased excretion of HCO<sub>3</sub><sup>-</sup> (bicarbonate), because the filtered load of HCO<sub>3</sub><sup>-</sup> exceeds the ability of the renal tubule to reabsorb it.


==Epidemiology and Demographics==
==Epidemiology and Demographics==

Revision as of 14:23, 16 May 2018




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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.D. [2]

Overview

Metabolic alkalosis is an elevation of the pH in the bloodstream which results from decreased hydrogen ion concentration leading to increased bicarbonate and carbon dioxide concentrations, or alternatively a direct result of increased bicarbonate concentrations.

Epidemiology and Demographics

It is the most common acid-base disorder seen in hospital in the United States.

Causes

Low urine chloride (<10mEq/dl)

  • Patients with low urine chloride and metabolic alkalosis respond well to treatment with volume repletion with saline, thus these conditions are often referred as saline-responsive metabolic alkalosis. Some conditions of volume depletions are:
  • Other condition with similar presentation but without volume depletion is hypercapnia

Normal urine chloride (> 10mEQ/dL)

Common Causes

Causes by Organ System

Cardiovascular Dilated cardiomyopathy, Malignant hypertension, Renovascular hypertension
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Aldosterone, Carbenoxolone, Diuretics, Ethacrynic Acid, Fludrocortisone, Glucocorticoids, Intravenous Pencillins, Laxatives, Lydia Pinkham's vegetable compound, Mineralocorticoids, Pramipexole, Sodium bicarbonate, Tolazoline, Tromethamine
Ear Nose Throat No underlying causes
Endocrine Cushing syndrome, Glucocorticoid-remediable hyperaldosteronism, Hyperaldosteronism, 11 beta hydroxylase deficiency, C17-hydroxylase deficiency, Conn syndrome, Bilateral adrenal hyperplasia, Adrenal adenoma, Adrenal carcinoma
Environmental No underlying causes
Gastroenterologic Gastric fistula, Villous adenoma, VIPoma, Congenital chloride diarrhea, Cystic fibrosis
Genetic 11 beta hydroxylase deficiency, Bartter syndrome, C17-hydroxylase deficiency, Congenital chloride diarrhea, Cystic fibrosis, Gietelman syndrome, Glucocorticoid receptor defect, Liddle syndrome, SeSAME syndrome
Hematologic No underlying causes
Iatrogenic Massive blood transfusion, Nasogastric suction
Infectious Disease No underlying causes
Musculoskeletal / Ortho No underlying causes
Neurologic No underlying causes
Nutritional / Metabolic Hypercalcemia, Hypokalemia, Hypomagnesemia, Refeeding syndrome, Glucocorticoid receptor defect, Glycyrrhizic acid, Licorice
Obstetric/Gynecologic No underlying causes
Oncologic Adrenal adenoma, Adrenal carcinoma, Conn syndrome, Hemangiopericytoma,VIPoma, Juxtaglomerular cell tumor
Opthalmologic No underlying causes
Overdose / Toxicity Aldosterone, Carbenoxolone, Diuretics, Fludrocortisone, Glucocorticoids, Intravenous Pencillins, Laxatives, Lydia Pinkham's vegetable compound, Mineralocorticoids, Sodium bicarbonate, Tolazoline, Tromethamine
Psychiatric No underlying causes
Pulmonary Cystic fibrosis
Renal / Electrolyte Bilateral adrenal hyperplasia, Hypokalemic distal renal tubular acidosis, Juxtaglomerular cell tumor, Milk-alkali syndrome, Renovascular hypertension, Bartter syndrome, Gietelman syndrome, Liddle syndrome, Adrenal adenoma, Adrenal carcinoma
Rheum / Immune / Allergy No underlying causes
Sexual Cystic fibrosis
Trauma No underlying causes
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Chewing tobacco, Glycyrrhizic acid, Licorice, Posthypercapnia, Vomiting, Laxatives, Refeeding syndrome, Milk-alkali syndrome

Causes in Alphabetical Order


References

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