Tuesday, August 2, 2016

Approach to acid base disorders: Metabolic alkalosis notes

In suspected metabolic alkalosis, always check urinary chloride levels.

Metabolic alkalosis associated with a reduction in the ECV (Vomiting, diuretics):
There will be a stimulus for Na and Cl reabsorption to replenish extracellular volume.
Urinary Cl is very low ( < 25 meq/L).
Administration of NaCl and water leads to correction of the metabolic alkalosis.
Such causes of metabolic alkalosis are said to be saline responsive.
Metabolic alkalosis associated with an expanded volume state (Mineralocorticoid excess, Barrters, Gitelman syndrome):
There is no stimulus for Na and Cl reabsorption.
The urinary Cl will be high ( > 40 meq/L).
Administration of saline would not correct the alkalosis.
Such causes of metabolic alkalosis are said to be saline resistant.

Check blood pressure in saline resistant metabolic alkalosis:
Mineralocorticoid excess states tend to be associated with hypertension.
Exogenous alkali load, Barrters and Gitelman's syndrome are associated with normal blood pressure.

Checking bicarbonate levels:
I had an interesting practice question about an anorexic bulimic patient, the tough part was differentiating alkalosis due to vomiting and alkalosis due to laxative abuse.
They can be differentiated on the bicarbonate levels.
Laxative abuse can decrease HCO3- because you are pooping bicarb out.
Vomiting will cause a relative increase in HCO3- levels.

For the sake of completion, I am enumurating all causes of matabolic alkalosis I can think of and dividing them into saline responsive and saline resistant :)

Causes of low urine chloride:
Gastrointestinal loss of hydrogen
Removal of gastric secretions: Vomiting or nasogastric suction
Chloride-losing diarrhea
Villous adenoma
Contraction alkalosis
Remote diuretic use (Loop or thiazide-type diuretics)
Sweat and urinary losses in cystic fibrosis
Gastric losses in achlorhydria

Causes of high urine chloride:
Mineralocorticoid excess:
Primary Aldosteronism
Cushings syndrome
AR kidney disorders:
Bartter's syndrome
Gitelman's syndrome
Current diuretic use (Loop or thiazide-type diuretics)
Decreased magnesium

That's all!
Metabolic alkalosis is simpler compared to metabolic acidosis ^__^
Metabolic acidosis can make you cry T_T

Related posts:
Bartters, Gitelmans and Liddles syndrome mnemonic
Metabolic acidosis notes
Normal arterial blood gas values mnemonic

PS: Many of you ask me where to study acid base and electrolytes disorders from, I think this Acid base online tutorial by Timur Graham and Steven Agnus, University of Connecticut is the best free resource for everyone.


  1. Thanks for the amazing post.
    Mineralocorticoid excess does have Na absorption. Only that Chloride absorption is compromised.
    Secondly with laxative abuse you're popping bicarb out so naturally wouldn't that lead to acidosis as opposed to alkalosis written here.

    1. You're most welcome.

      Regarding mineralocorticoid excess:
      Aldosterone acts on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it upregulates and activates the basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of sodium (Na+) ions and water (which follows sodium) into the blood, and secreting potassium (K+) ions into the urine (lumen of collecting duct).
      Source: https://en.wikipedia.org/wiki/Aldosterone

      Regarding laxative abuse:
      Long term laxative ingestion causes increased and unregulated losses of K+.
      If this excess loss is not counterbalanced by a concomitant increase in dietary K+ intake, then body K+ stores will become depleted, a change that causes hypokalemia and some H+ shift into cells, raising extracellular fluid [HCO3−].
      The increase in [HCO3−] may be sustained by the effect of K+ depletion to increase renal NH4+ production and excretion.
      The major clinical feature of laxative abuse is hypokalemia; clinically significant metabolic alkalosis, if present, is usually mild.
      If laxative abuse induces excessive diarrheal losses, then metabolic acidosis can of course occur, as with any severe diarrhea.
      Source: http://cjasn.asnjournals.org/content/3/6/1861.full


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