Metabolic alkalosis generation

Metabolic acidosis and metabolic alkalosis are generated by a primary change in the serum bicarbonate concentration. In metabolic acidosis, bicarbonate is lost or a nonvolatile acid is gained, whereas metabolic alkalosis is characterized by a gain in bicarbonate or a loss of nonvolatile acid. 

Metabolic alkalosis is a simple acid-base disorder that presents as al-kalemia (increased arterial pH) with an increase in plasma bicarbonate. It is an extremely common entity in hospitalized patients with acid-base disturbances. Under normal circumstances, the kidney is readily able to excrete an alkali load. Thus evaluation of patients with metabolic alkalosis must consider two separate issues (1) the initial process that generates the metabolic alkalosis and (2) alterations in renal function that maintain the alkalemic state. °... 

Henle (e.g., furosemide, bumetanide, and torsemide) and distal convoluted tubule (thiazides), have most commonly been associated with the generation of metabolic alkalosis. These agents promote the excretion of sodium and potassium almost exclusively in association with chloride, without a proportionate increase in bicarbonate excretion. Collecting duct hydrogen ion secretion is stimulated directly by the increased luminal flow rate and sodium delivery, and indirectly by intravascular volume contraction, which results in secondary hyperaldosteronism. Renal ammoniagenesis may also be stimulated by concomitant hypokalemia, further augmenting net acid excretion. 

Metabolic alkalosis may also be generated by the gain of exogenous alkali. This may be seen as a result of bicarbonate administration or from the infusion of organic anions that are metabolized to bicarbonate, such as acetate, lactate, and citrate. The milk-alkali syndrome was historically a common cause of metabolic alkalosis in patients with peptic ulcer disease secondary to the ingestion of large quantities of milk products and antacids. This syndrome has become increasingly uncommon with the advent of alternative effective therapies for dyspeptic syndromes. 

Mineralocorticoid excess also plays a significant role in the maintenance of metabolic alkalosis. In patients with volume-responsive metabolic alkalosis, intravascular volume depletion stimulates aldosterone secretion. As discussed earlier, excess mineralocorticoid activity may also underlie the generation of metabolic alkalosis. In either situation, the increased mineralocorticoid effect stimulates collecting duct H+ secretion. Metabolic alkalosis may also be maintained by persistent hypokalemia. Hypokalemia has a multitude of effects on renal acid-base homeostasis, enhancing proximal tubular bicarbonate reabsorption, stimulating ammoniagenesis and increasing distal tubular H secretion. ... 

This mixed disorder often occurs in patients with chronic obstructive pulmonary disease and chronic respiratory acidosis who are treated with salt restriction, dinretics, and possibly glncocorticoids. When diuretics are initiated, the plasma bicarbonate may increase because of increased renal bicarbonate generation and reabsorption, providing mechanisms for both generating and maintaining metabolic alkalosis. The elevated pH diminishes respiratory drive and may therefore worsen the respiratory acidosis. 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

Human blood has a normal pH of 7.35 to 7.45. Any deviation horn this range can have extremely disruptive effects on the stability of cell membranes, the structures of proteins, and the activities of enzymes. Death may result if the blood pH falls below 6.8 or rises above 7.8. When the pH falls below 7.35, the condition is called acidosis when it rises above 7.45, the condition is called alkalosis. Acidosis is the more common tendency because metabolism generates several acids in the body. 

When the pH falls below 7.35, the condition is called acidosis when it rises above 7.45, the condition is called alkalosis. Acidosis is the more common tendency because ordinary metabolism generates several acids within the body. 

---