Alkalosis
Metabolic alkalosis split by urine chloride and blood pressure, how it is maintained and corrected, and the causes and compensation of respiratory alkalosis.
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Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Metabolic alkalosis is a primary rise in bicarbonate (above about 28 mmol/L). It is the commonest acid-base disorder in hospital, mostly from diuretics and vomiting.
- Two steps keep it going: something generates it (acid loss or alkali gain), and something stops the kidney excreting the excess (volume and chloride depletion, hypokalaemia or mineralocorticoid excess).
- Split it by urine chloride and blood pressure. That one step sorts nearly every cause.
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Sources
- Emmett M. Metabolic alkalosis: a brief pathophysiologic review. Clin J Am Soc Nephrol 2020;15:1848-56Clinical Journal of the American Society of Nephrology, 2020
- Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med 2014;371:1434-45New England Journal of Medicine, 2014
- Mullens W et al. Acetazolamide in acute decompensated heart failure with volume overload (ADVOR). N Engl J Med 2022;387:1185-95New England Journal of Medicine, 2022
- Faisy C et al. Effect of acetazolamide vs placebo on duration of invasive mechanical ventilation among patients with COPD (DIABOLO). JAMA 2016;315:480-8JAMA, 2016
- Adler GK et al. Primary aldosteronism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2025;110:2453-95Endocrine Society, 2025
- Blanchard A et al. Gitelman syndrome: consensus and guidance from a KDIGO Controversies Conference. Kidney Int 2017;91:24-33Kidney Disease Improving Global Outcomes, 2017
- Last updated
- 14 November 2026
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