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Metabolic alkalosis

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Subject: Base excess, Respiratory alkalosis, Diuretic, Respiratory compensation, Alkaline tide
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Metabolic alkalosis

Metabolic alkalosis
Classification and external resources
Specialty Endocrinology
ICD-10 E87.3
ICD-9-CM 276.3
DiseasesDB 402
eMedicine med/1459

Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35-7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.


  • Terminology 1
  • Causes 2
    • Chloride-responsive (Urine chloride < 20 mEq/L) 2.1
    • Chloride-resistant (Urine chloride > 20 mEq/L) 2.2
  • Compensation 3
  • See also 4
  • References 5


  • Alkalosis refers to a process by which the pH is increased.
  • Alkalemia refers to a pH which is higher than normal, specifically in the blood.


The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels.[1]

Chloride-responsive (Urine chloride < 20 mEq/L)

  • Loss of hydrogen ions - Most often occurs via two mechanisms, either vomiting or via the kidney.
    • Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes.
    • Severe vomiting also causes loss of potassium (hypokalaemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.[2]
  • Congenital chloride diarrhea - rare for being a diarrhea that causes alkalosis instead of acidosis.
  • 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 increased concentration of bicarbonate "mops up" more of the hydrogen ions and raises the blood pH.
    • Diuretic therapy - loop diuretics and thiazides can both initially cause increase in chloride, but once stores are depleted, urine excretion will be below < 25 mEq/L. The loss of fluid from sodium excretion causes a contraction alkalosis.
  • Posthypercapnia - Hypoventilation (decreased respiratory rate) causes hypercapnia (increased levels of CO2), which results in respiratory acidosis. Renal compensation with excess bicarbonate occurs to lessen the effect of the acidosis. Once carbon dioxide levels return to base line, the higher bicarbonate levels reveal themselves putting the patient into metabolic alkalosis.
  • Cystic Fibrosis

Chloride-resistant (Urine chloride > 20 mEq/L)

  • Retention of bicarbonate - retention of bicarbonate would lead to alkalosis
  • Shift of hydrogen ions into intracellular space - Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.
  • Alkalotic agents - Alkalotic agents, such as bicarbonate (administrated in cases of peptic ulcer or hyperacidity) or antacids, administered in excess can lead to an alkalosis.
  • Hyperaldosteronism - Renal loss of hydrogen ions occurs when excess aldosterone (Conn's syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine.[3]
  • Excess Glycyrrhizin consumption
  • Bartter syndrome and Gitelman syndrome - syndromes with presentations analogous to taking diuretics characterized with normotensive patients
  • Liddle syndrome - a syndrome from defect sodium channel deletion characterized by hypertension and hypoaldosteronism.
  • 11β-hydroxylase deficiency and 17α-hydroxylase deficiency - both characterized by hypertension
  • Aminoglycoside toxicity can induce a hypokalemic metabolic alkalosis via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartter's syndrome like effect.


Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO2) through slower breathing, or hypoventilation (respiratory compensation). CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Respiratory compensation, though, is incomplete. The decrease in [H+] suppresses the peripheral chemoreceptors, which are sensitive to pH. But, because respiration slows, there's an increase in pCO2 which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO2 in the cerebral spinal fluid. So, because of the central chemoreceptors, respiration rate would be increased.

Renal compensation for metabolic alkalosis, less effective than respiratory compensation, consists of increased excretion of HCO3 (bicarbonate), as the filtered load of HCO3 exceeds the ability of the renal tubule to reabsorb it.

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used:

  • pCO2 = 0.7 [HCO3] + 20 mmHg +/- 5
  • pCO2 = 0.7 [HCO3] + 21 mmHg [4]

See also


  1. ^
  2. ^ Hennessey, Iain. Japp, Alan.Arterial Blood Gases Made Easy. Churchill Livingstone 1 edition (18 Sep 2007).
  3. ^ Cho Kerry C, "Chapter 21. Electrolyte & Acid-Base Disorders" (Chapter). McPhee SJ, Papadakis MA: CURRENT Medical Diagnosis & Treatment 2011:
  4. ^ Hasan, Ashfaq. "The Analysis of Blood Gases." Handbook of Blood Gas/Acid-Base Interpretation. Springer London, 2013. pp. 253-266.
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