What is the impact of a deficit of H + and Cl −
Removal of HCl from the stomach was first studied in seminal experiments performed by Schwartz and Kassirer. The initial loss of gastric contents is considered the generation phase for metabolic alkalosis. A deficit of Cl − without a deficit of Na + or K + occurs. Based on electroneutrality, this must represent a deficit of an equimolar amount of H + . Hence there is a net gain of an equimolar amount of HCO 3 − in the body, causing alkalemia and a higher [HCO 3 − ]. Because gastric fluid contains relatively little Na + and K + , there are no important changes in Na + or K + balance. Hence there are no important changes in the ICF compartment, merely a loss of Cl − and an equivalent gain of HCO 3 − in the ECF compartment.
When the deficit is purely HCl, one could, in theory, give HCl to the patient. This choice is rarely made, because the administration of HCl via intravenous infusion is somewhat inconvenient. Alternatively, one could give NaCl, because the expanded ECF volume will result in the excretion of the administered Na + with the extra HCO 3 − that was present in the ECF compartment. The administered Cl − will be retained.
However, as this initial period of gastric acid loss persists, additional events occur before the steady state develops. The rise in serum [HCO 3 − ] leads to an increase in filtered [HCO 3 − ]. This is because sodium is not yet lost and there is not a significant stimulus for renin and angiotensin II; consequently, there is little bicarbonate reabsorption in the PCT. Bicarbonaturia ensues, demonstrated by an increase in the urine pH, and obligating loss of Na + and K + . The loss of extracellular fluid volume (ECFV) and the development of hypokalemia are therefore the result of renal, not gastric, losses. Increased renin and angiotensin II then follow.
Untreated, even were the vomiting and loss of gastric fluid to stop, a maintenance period would follow. The deficiency of both Cl − and K + will prevent the excretion of the excess generated [HCO 3 − ]. During this phase, as the filtered HCO 3 − is reabsorbed in the PCT, there is no further bicarbonaturia, and the urine pH is acidic. This observation is the paradoxical aciduria of metabolic alkalosis, representing the failure of the kidneys to excrete the excess generated bicarbonate. Further urinary losses of Na + and K + do not occur. Because the deficit is now mostly of KCl, the administration of KCl is most important. Giving NaCl alone will not correct the deficit of KCl acutely. To the extent that the ECFV is contracted, administration of NaCl is appropriate and will allow suppression of renin and angiotensin II. Repletion of Cl − allows the kidneys to reabsorb Na + with Cl − instead of HCO 3 − , and repletion of K + suppresses other mechanisms associated with bicarbonate reabsorption discussed previously.
