Pathophysiology of Metabolic Alkalosis               <A-MetAlk.TXT>
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PRIMARY EVENT   The primary event is either loss of H+ or gain of HCO3-.
Examples: upper GI losses from vomiting or NG suction, H+ loss from the kidney.
Or, H+ may move into the cells because of a low serum K+.  Alkalosis may also
result from addition of HCO3- or (purportedly) "contraction" of fluid volume
around a fixed amount of HCO3-.

MAINTENANCE   Alkalosis will quickly be corrected by compensatory mechanisms
unless some factor is acting to maintain the alkalosis.  Several factors may
maintain an alkalosis, all by decreasing HCO3- excretion:

   A high aldosterone state, either primary or secondary <A-Aldo.TXT>

    K+ or  Cl- <A-K.TXT>

   The renal Tm for HCO3- may be reset  by all of the above, and by  volume.*

   Non-resorbable anions (e.g., penicillin, carbenicillin) take HCO3- with them.

    pCO2 secondary to alkalosis causes a TERTIARY renal HCO3- retention (up to
   40% of the  HCO3- in metabolic alkalosis may be secondary to this).**

   Renal failure with decreased HCO3- filtration (rare)
   
   A metabolic alkalosis (but not alkalemia) may be a compensatory loss of H+
   due to primary respiratory or metabolic acidosis. (Caused by  H+ in renal
   tubule cells.)

   (insert figure from Gardner, Textbook of Acute Internal Medicine, 1985, p.
      505)

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*Mechanism: increased H+ in renal tubule cells (because of K+ efflux in  K+)
 causes  H+ excretion.

**"Metabolic alkalosis", Harrington, John T., Kidney International, 26(1984)
 88-97.                                                            <A-Class.TXT>