Clinical Syndromes of Metabolic Alkalosis

Homeostatic control of acid–base parameters within discreet limits is vital to all living organisms. Acid–base disturbances are conditions that reflect abnormal underlying physiologic processes that can stem from a broad range of etiologies. In humans with a filtration-reabsorption nephron design, more than 4000 mEq of HCO 3 − is filtered daily at the glomerulus and virtually all of it is reabsorbed by the tubules.Two points are noteworthy. Since HCO 3 − absorption is an active process, in defense of elevated plasma [HCO 3 − ], the renal tubule simply has to do less work and bicarbonaturia invariably ensues. Given the relative magnitudes of filtered and reabsorbed versus excreted HCO 3 − , bicarbonaturia can be massive, which translates to rapid correction of excess extracellular fluid HCO 3 − . Within such context, one wonders why metabolic alkalosis would even be encountered. In contrast to metabolic acidosis, where the pathophysiology reflects increased acid production, reduced acid excretion, or both, the maintenance of metabolic alkalosis is a quintessential renal disease of altered HCO 3 − absorption.Alkalosis is the condition in which there is an excess of base in total body fluids. By contrast, alkalemia refers to a state of decreased H + activity in the plasma (reduced plasma pH). Alkalosis can exist without alkalemia because alkalosis might be part of a mixed acid–base disturbance. Conversely, alkalemia can be present without total body alkalosis. The adjective metabolic denotes that the disturbance is caused by a primary gain of base (e.g., HCO 3 − ) or loss of H + from the body.