Physiology · Renal, fluids and acid–base
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 · Stomach
What it is
Metabolic alkalosis is a primary rise in plasma HCO₃⁻. Two moments must be separated: what generated it (H⁺ loss through vomiting or the kidney, alkali gain, loss of bicarbonate-free fluid) and what maintains it, because a healthy kidney would excrete the excess within hours. It persists with volume or chloride depletion, hypokalaemia or mineralocorticoid excess. The lungs compensate by hypoventilating, a response limited by hypoxaemia.
How it works, step by step
- 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 | Low (< ≈20 mmol/L) | Reduced | Vomiting, nasogastric suction, diuretics already stopped, post-hypercapnia |
| Chloride-resistant, hypertensive | High | Normal or expanded | Hyperaldosteronism, Cushing syndrome, mineralocorticoid excess |
| Chloride-resistant, normotensive | High | Reduced or normal | Current diuretic use, Bartter and Gitelman syndromes, severe hypokalaemia |
Clinical notes
- 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.
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.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Renal handling of H⁺ and bicarbonate
- Reading an arterial blood gas step by step
- Mixed acid–base disorders
- Potassium balance
- Vomiting and its control
- Where and how diuretics act
Related conditions
In Biochemistry
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 (OpenStax (Rice University), 2022); Alkalosis: MedlinePlus Medical Encyclopedia (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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Representative model, for educational purposes only.