When the body loses gastric contents through vomiting or nasogastric suctioning, it leads to metabolic alkalosis due to the loss of hydrochloric acid (HCl). If there is a significant loss of gastric fluid, it causes contraction of the extracellular fluid volume (ECFV). In this condition, the kidneys are unable to excrete enough bicarbonate (HCO3−) to compensate for the metabolic alkalosis. This is because the kidneys need to reduce sodium (Na+) excretion to correct the ECFV contraction. As explained before, this response leads to a reduction in the glomerular filtration rate, which decreases the filtered load of HCO3− and increases Na+ reabsorption in the nephron. Since a large amount of Na+ reabsorption occurs through the Na+/H+ antiporter, it results in increased H+ secretion (HCO3− reabsorption) in the proximal tubule. In this situation, the entire filtered load of HCO3− is reabsorbed, and the generation of new HCO3− may even be enhanced. This occurs because aldosterone, which is elevated in volume contraction, not only stimulates distal Na+ reabsorption but also H+ secretion by intercalated cells. This stimulation of H+ secretion generates new HCO3− by enhancing titratable acid and NH4+ excretion. Therefore, in individuals who lose gastric contents, metabolic alkalosis and paradoxically acidic urine typically occur. The alkalosis is corrected only when euvolemia (normal body fluid volume) is restored.

Table 37.1 provides a summary of the primary alterations and compensatory or defense mechanisms in different acid-base disorders. The compensatory response in all acid-base disorders does not correct the underlying problem but rather reduces the extent of the pH change. To correct the acid-base disorder, the cause of the problem needs to be treated.

Metabolic acidosis is characterized by a decrease in extracellular fluid (ECF) concentration of bicarbonate [HCO3−] and pH. It can develop from the addition of nonvolatile acid to the body (e.g., diabetic ketoacidosis), loss of nonvolatile base (e.g., HCO3− loss due to diarrhea), or failure of the kidneys to excrete titratable acid and NH4+ (e.g., renal failure). As mentioned earlier, the buffering of H+ occurs in both the ECF and intracellular fluid (ICF) compartments. When the pH decreases, the respiratory centers are stimulated, leading to an increased ventilatory rate as a compensatory response.

In metabolic acidosis, renal net acid excretion (RNAE) is increased. This occurs through the elimination of all HCO3− from urine (enhanced reabsorption of filtered HCO3−) and increased excretion of titratable acid and NH4+ (enhanced production of new HCO3−). If the process that caused the acid-base disturbance is corrected, the enhanced RNAE will eventually restore the pH and [HCO3−] to normal. After the pH is corrected, the ventilatory rate also returns to normal.

Metabolic alkalosis is characterized by an increase in ECF concentration of bicarbonate [HCO3−] and pH. It can occur due to the addition of nonvolatile base to the body (e.g., ingestion of antacids), volume contraction (e.g., hemorrhage), or more commonly, the loss of nonvolatile acid (e.g., loss of gastric HCl through prolonged vomiting). Buffering mainly occurs in the ECF and to a lesser extent in the ICF.
Lossofgastriccontentsfromthebody(e.g.,vomiting,nasogastricsuctioning)producesmetabolicalkalosissecondarytothelossofHCl.Ifthelossofgastricfluidissignificant,ECFVcontractionoccurs.UnderthisconditionthekidneyscannotexcretesufficientquantitiesofHCO3− tocompensateforthemetabolicalkalosis.TheinabilityofthekidneystoexcreteHCO3− isaresultoftheneedtoreduceNa+ excretiontocorrecttheECFVcontraction.Asdescribedpreviously(see fordetails)theresponseofthekidneystovolumecontractionistoreducetheglomerularfiltrationrate,whichreducesthefilteredloadofHCO3− ,andtoincreaseNa+ reabsorptionalongthenephron.BecausealargeamountofNa+ reabsorptionoccursviatheNa+/H+ antiporter,thisresultsinanincreaseinH+ secretion(HCO3− reabsorption)bytheproximaltubule.InthissettingtheentirefilteredloadofHCO3− isreabsorbedandnewHCO3− generationmayevenbeenhanced.Thelatterresponseoccursbecausealdosterone,thelevelsofwhichareelevatedinvolumecontraction,notonlystimulatesdistalNa+ reabsorptionbutalsoH+ secretionbyintercalatedcells.ThisstimulationofH+ secretiongeneratesnewHCO3− byenhancingtitratableacidandNH4+ excretion.Thusinindividualswholosegastriccontents,metabolicalkalosisandparadoxicallyacidicurinecharacteristicallyoccur.Correctionofthealkalosisoccursonlywheneuvolemiaisreestablished.
Table 37.1 summarizes the primary alterations and the subsequent compensatory or defense mechanisms of the various simple acid-base disorders. In all acid-base disorders the compensatory response does not correct the underlying disorder but simply reduces the magnitude of the change in pH. Correction of the acid-base disorder requires treatment of its cause.
Types of Acid-Base Disorders
Metabolic acidosis is characterized by a decreased ECF [HCO3 −] and pH. It can develop via the addition of nonvolatile acid to the body (e.g., diabetic ketoacidosis), the loss of nonvolatile base (e.g., HCO3 − loss caused by diarrhea), or failure of the kidneys to excrete titratable acid and NH4 + (e.g., renal failure). As previously described, the buffering of H+ occurs in both the ECF and ICF compartments. When the pH falls, the respiratory centers are stimulated and the ventilatory rate is increased (respiratory compensation).
Finally, in metabolic acidosis, RNAE is increased. This occurs via elimination of all HCO3 − from urine (enhanced reabsorption of filtered HCO3 −) and via increased titratable acid and NH4 + excretion (enhanced production of new HCO3 −). If the process that initiated the acid-base disturbance is corrected, the enhanced RNAE will ultimately return the pH and [HCO3 −] to normal. After correction of the pH, the ventilatory rate also returns to normal.
Metabolic alkalosis is characterized by an increased ECF [HCO3 −] and pH. It can occur via the addition of nonvolatile base to the body (e.g., ingestion of antacids), as a result of volume contraction (e.g., hemorrhage), or more commonly from loss of nonvolatile acid (e.g., loss of gastric HCl because of prolonged vomiting). Buffering occurs predominantly in the ECF and to a lesser degree in the
Respiratoryacidosis↓ Respiratoryalkalosis↑ ECF,extracellularfluid;ICF,intracellularfluid;RNAE,renalnetacidexcretion