Metabolic Alkalosis

Adam M. Franks and Joseph I. Shapiro Recommended Time to Complete: 1 Day

Guiding Questions

  • 1. What is metabolic alkalosis and how does it occur?
  • 2. What are the compensatory mechanisms for metabolic alkalosis?
  • 3. How is metabolic alkalosis maintained?
  • 4. What are the clinical features of metabolic alkalosis?
  • 5. How does one differentiate various causes of metabolic alkalosis?
  • 6. How does one treat metabolic alkalosis?

Metabolic alkalosis is an acid-base disorder that occurs as the result of a process that increases pH (alkalemia) from a primary increase in serum bicarbonate concentration ([HCO-]). The primary elevation of serum [HCO-] is caused by the pathophysiologic processes outlined below.

Net H+ Loss from Extracellular Fluid

A loss of protons from the body occurs primarily through either the kidneys or the gastrointestinal (GI) tract. When H+ losses exceed the daily H+ load produced by metabolism and diet, a net negative H+ balance results. Because the H+ loss results in the generation of a HCO-, increases in serum [HCO-] result. GI loss of protons generally occurs in the stomach; in this setting, H+ secretion by the luminal gastric parietal cell H+ -adenosine triphosphatase (ATPase) leaves a HCO- to be reclaimed at the basolateral surface. The coupling between net acid excretion (NAE) and bicarbonate generation in the kidney was discussed at length in Chapter 7 . Finally, H+ shifts into cells may accompany significant potassium depletion. Again, this should produce a rise in extracellular fluid (ECF) [HCO-]. Regarding this last mechanism, we should point out that evidence of intracellular acidosis developing during experimental potassium depletion has not been consistently observed in experimental settings, and it is certainly possible that increases in NAE serves as the predominant mechanism for metabolic alkalosis with potassium deficiency.

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