Question 4 from the second paper of 2006 asks the candidates to discuss the management of metabolic alkalosis. The college offers an uninspired answer in point form. Though adequate from a pass-the-exam technical standpoint, this does not satisfying for anybody who actually wants to understand why they are doing the things they are doing.  This chapter aims to expand on the physiology involved in the correction of metabolic alkalosis, beyond the simple act of giving more acid.

A good article on metabolic alkalosis in ICU was published by Webster and Kulkarni in 1999. According to them, treatment of metabolic alkalosis consists of three essential components.  Correct the aetiology of the bicarbonate retention (eg. the volume deficit), correct the source of chloride loss (be it diarrhoea or NG drainage) and correct co-existing electrolyte abnormalities (eg. potassium and magnesium). "Specific therapy may be viewed as either measures to achieve removal of base or those that increase the supply of acid", say the authors. The article then goes on to offer a classical pre-Stewart interpretation of metabolic alkalosis, which is probably still acceptable for routine work. However, these days college seems to be trending in the direction of quantitative acid-base interpretation. This is attempted with a satisfying attention to detail in a relatively recent article from the Indian Society of Critical Care (Tripathi, 2009).  Three slightly different essential steps are recommended in the more recent (2015) UpToDate article on this topic: Correct true volume depletion, correct potassium depletion. and correct chloride depletion. UpToDate authors do not seem bothered about the underlying disorder.  I have synthesised both articles into one point-form list.


  • Correct volume depletion - ideally with normal saline
    • Volume and chloride depletion are both corrected by normal saline. However, you can give free water and still get away with it.
      Volume depletion contributes to alkalosis by creating a stimulus for sodium retention, which in turn increases the strong ion difference. By removing this stimulus, normal sodium excretion can occur, which works to shrink the SID back to a normal level. This can be accomplished by any damn fluid, be it 5% dextrose or cheap red wine.
    • Moreover, fresh water has an SID of zero, which means that giving it to a patient with a large SID will have am SID-reducing effect (and therefore correct the alkalosis). Infusion of a zero-SID fluid will therefore crudely correct the SID in the alkalotic patient.
    • However, by offering a chloride-rich replacement fluid, we can also increase the delivery of chloride to the cortical collecting duct, where chloride and bicarbonate are exchanged (thus increasing bicarbonate excretion).
    • Normal saline also has an SID of zero, which means that it will crudely correct the SID when infused into the alkalotic patient.
    • Thus, replacement of volume with normal saline is ideal, as it not only corrects the immediate biochemical problem, but also promotes normal acid-base behaviour at the nephron.
    • The effectiveness of this strategy can be tested by measuring the urine pH, which should trend towards the alkaline range (pH >7.0) as the saline boluses are given.
  • Correct hypokalemia - ideally with potassium chloride
    • Hypokalemia is harmful in a cardiovascular sense, but that is beside the point.
    • Potassium is exchanged for H+ at the cellular membrane to maintain electroneutrality; the replacement of potassium therefore encourages the migration of H+ out of cells, theoretically resulting in a decrease of extracellular pH as the H+ is buffered by HCO3-
    • Movement of H+ out of cells raises the intracellular pH, which in renal tubular cells causes a decrease in the rate of bicarbonate reabsorption.
    • The replacement of potassium losses also reverses the hypokalemia-induced stimulation of the distal H-K-ATPase, an ATP powered pump which reabsorbs potassium in exchange for excreting H+.
    • Potassium replacement should be as chloride salt (KCl)
  • Alternative strategies if the patient is fluid-overloaded:
    • Acetazolamide (prevent reabsorption at the proximal tubule)
    • Hydrochloric acid (HCl)
    • Infusions of cationic amino acids such as lysine and arginine - these amino acids are typically available a hydrochloride solutions; when they are metabolised, only chloride remains.
    • Correction of hypoalbuminaemia (albumin is anionic, and together with phosphate represents Atot; hypoalbuminaemia contributes to alkalosis)


Tripathy, Swagata. "Extreme metabolic alkalosis in intensive care." Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine 13.4 (2009): 217.


Galla, John H. "Metabolic alkalosis." Journal of the American Society of Nephrology 11.2 (2000): 369-375.

Pahari, D. K., et al. "Diagnosis and management of metabolic alkalosis."JOURNAL-INDIAN MEDICAL ASSOCIATION 104.11 (2006): 630.


Palmer, Biff F., and Robert J. Alpern. "Metabolic alkalosis." Journal of the American Society of Nephrology 8.9 (1997): 1462-1469.


Gennari, F. John. "Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport." American Journal of Kidney Diseases 58.4 (2011): 626-636.


Ferrara, A., et al. "[Physiopathological and clinical data on post-hypercapnic metabolic alkalosis. A case of severe hypercapnia treated with drugs and in an" iron lung"]." Minerva medica 70.1 (1979): 67-73.


Banga, Amit, and G. C. Khilnani. "Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay." COPD: Journal of Chronic Obstructive Pulmonary Disease 6.6 (2009): 437-440.

Webster, Nigel R., and Vivek Kulkarni. "Metabolic Alkalosis in the Critically III." Critical reviews in clinical laboratory sciences 36.5 (1999): 497-510.