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[Physiology](https://durgical.com/en/physiology/) · [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal)

# Metabolic alkalosis and its compensation

- Mechanism
- Exam priority: medium

When there is too much bicarbonate in the blood, pH rises; the lungs breathe less to compensate and the kidney decides whether to fix it or keep it.

Updated 2026-11-01

Also called: Contraction alkalosis, Hypochloraemic alkalosis

**See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/) · [Stomach](https://durgical.com/en/anatomy/stomach/)

## Key points

- Generation vs maintenance: without a maintaining factor, the kidney excretes surplus HCO₃⁻ quickly.
- Maintaining factors: volume, Cl⁻ and K⁺ depletion, and high aldosterone.
- Vomiting or nasogastric suction: hypochloraemic, hypokalaemic alkalosis; K⁺ is lost mostly in urine (aldosterone), not in vomit.
- Low urine chloride (
- Vomiting removes HCl from the stomach; for each H⁺ lost, the parietal cell has already released one HCO₃⁻ into the blood.
- As filtered HCO₃⁻ rises, the kidney would start excreting it (alkaline urine with Na⁺ and K⁺).
- But volume loss activates angiotensin II and aldosterone: the proximal tubule reclaims more HCO₃⁻ and the collecting duct secretes H⁺ and K⁺.
- Chloride lack stops pendrin in β-intercalated cells from exchanging Cl⁻ for HCO₃⁻: bicarbonate cannot get out.
- Hypokalaemia shifts H⁺ into cells and stimulates H⁺ secretion and ammoniagenesis: the alkalosis perpetuates itself.
- The respiratory centre senses the high pH and reduces ventilation: PaCO₂ rises and pH moves toward normal without reaching it.
- Once volume and chloride are restored, the kidney excretes bicarbonate again and the alkalosis resolves.

## Two groups by urine chloride

| Group | Urine chloride | Volume | Examples |
| --- | --- | --- | --- |
| [Chloride-responsive](https://durgical.com/en/conditions/infantile-hypertrophic-pyloric-stenosis/) | Low (
- Infantile hypertrophic pyloric stenosis: projectile non-bilious vomiting with hypochloraemic, hypokalaemic alkalosis.
- Alkalosis increases calcium binding to albumin: ionised calcium falls, with paraesthesiae, cramps or tetany.
- Compensatory hypoventilation rarely pushes PaCO₂ much beyond ≈55 mmHg: hypoxaemia limits how much ventilation can be cut.

## Memory aid

“To dump alkali, the kidney needs salt and potassium”: without chloride and volume it keeps the bicarbonate, however much there is.

## Test yourself

Think of the answer, then tap the question to see it.

## Why does a patient with persistent vomiting lose potassium mainly in the urine rather than in the vomit?

Gastric juice contains little K⁺. Volume loss raises aldosterone, and more distal Na⁺ and HCO₃⁻ delivery boosts collecting-duct K⁺ secretion: kaliuresis explains the hypokalaemia.

## What is the paradoxical aciduria of vomiting-induced alkalosis, and what causes it?

Acid urine with alkaline blood. Volume and K⁺ depletion force the collecting duct to reabsorb Na⁺ in exchange for H⁺ (and K⁺) secretion, driven by aldosterone.

## A hypertensive patient has metabolic alkalosis, hypokalaemia and a urine chloride of 60 mmol/L. What mechanism is suggested?

Mineralocorticoid excess (e.g. hyperaldosteronism): volume is expanded, urine Cl⁻ is high and the collecting duct secretes H⁺ and K⁺ autonomously; it does not respond to saline.

## Why is respiratory compensation for metabolic alkalosis limited?

Hypoventilation lowers PaO₂: hypoxaemia stimulates peripheral chemoreceptors and puts a ceiling on how far PaCO₂ can rise.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/metabolic-alkalosis-and-its-compensation/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Stomach](https://durgical.com/en/anatomy/stomach/)

## Related topics

- [Renal handling of H⁺ and bicarbonate](https://durgical.com/en/physiology/renal-handling-of-h-and-bicarbonate/)
- [Reading an arterial blood gas step by step](https://durgical.com/en/physiology/reading-an-arterial-blood-gas-step-by-step/)
- [Mixed acid–base disorders](https://durgical.com/en/physiology/mixed-acid-base-disorders/)
- [Potassium balance](https://durgical.com/en/physiology/potassium-balance/)
- [Vomiting and its control](https://durgical.com/en/physiology/vomiting-and-its-control/)
- [Where and how diuretics act](https://durgical.com/en/physiology/where-and-how-diuretics-act/)

## Related conditions

- [Metabolic alkalosis](https://durgical.com/en/conditions/metabolic-alkalosis/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Infantile hypertrophic pyloric stenosis](https://durgical.com/en/conditions/infantile-hypertrophic-pyloric-stenosis/)
- [Cushing syndrome](https://durgical.com/en/conditions/cushing-syndrome/)
- [Hypocalcaemia](https://durgical.com/en/conditions/hypocalcaemia/)

## In Biochemistry

- [Acid–base compensation rules](https://durgical.com/en/biochemistry/topics/acid-base-compensation-rules/)
- [Acid–base interpretation (step by step)](https://durgical.com/en/biochemistry/topics/acid-base-interpretation/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [26.5 Disorders of Acid-Base Balance](https://openstax.org/books/anatomy-and-physiology-2e/pages/26-5-disorders-of-acid-base-balance) (OpenStax (Rice University), 2022); [Alkalosis: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001183.htm) (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 31). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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