Metabolic alkalosis
is a relatively common clinical disorder that is most often due to diuretic therapy or the loss of gastric secretions due to vomiting (which may be surreptitious) or gastric suction. (See 'Introduction' above.)
The generation and subsequent maintenance of metabolic alkalosis require two separate factors (see 'Pathogenesis' above):
Elevation of the plasma bicarbonate concentration can be generated by excessive hydrogen ion loss into the urine or from the gastrointestinal tract, hydrogen ion movement into the cells, the administration of bicarbonate salts (or other alkalinizing salts such as sodium acetate or lactate), or volume contraction around a relatively constant amount of extracellular bicarbonate (called a contraction alkalosis).
•A decrease in renal bicarbonate excretion may be due to reduced kidney function, increased renal bicarbonate reabsorption, or reduced bicarbonate secretion.
Several factors are responsible for increased net renal bicarbonate reabsorption in metabolic alkalosis. In the absence of advanced kidney failure, one or more of these factors must be present to sustain the high plasma bicarbonate concentration:
•A reduction in extracellular fluid (ECF) volume or reduced effective arterial blood volume, including reduced tissue (and renal) perfusion in edematous states such as congestive heart failure and cirrhosis.
•Chloride depletion and hypochloremia.
•Hypokalemia.
•Increased distal nephron delivery and reabsorption of sodium ions in exchange for hydrogen and potassium ions.
No comments:
Post a Comment