Which of the following statements(s) is/are true concerning metabolic alkalosis?

b. In metabolic alkalosis secondary to prolonged gastric outlet obstruction, the urine pH is usually acidic

c. Hypokalemia can lead to metabolic alkalosis

d. The respiration compensatory mechanisms for metabolic alkalosis are quite ineffective

Sustained metabolic alkalosis occurs only if extracellular bicarbonate concentration is increased and renal excretion of excess bicarbonate is inhibited. Alone, neither is sufficient to result in metabolic alkalosis. Extracellular bicarbonate concentration is increased by numerous mechanisms. Loss of HCl is the leading cause of metabolic alkalosis in surgical patients. External loss of gastric acid results in net gain in bicarbonate, which causes metabolic alkalosis. Although the kidney can excrete excess bicarbonate, this must be accompanied by excretion of sodium. Renal excretion of sodium is limited in the face of volume depletion, which also occurs with external losses of gastric secretion. As volume depletion progresses, sodium is conserved in exchange for hydrogen. Thus, in metabolic alkalosis secondary to prolonged gastric outlet obstruction, the urine, although initially alkalotic, becomes paradoxically acidotic in prolonged or uncorrected cases. Hypokalemia and cellular exchange of potassium for hydrogen can also lead to metabolic alkalosis. Hypokalemia results in enhanced proximal tubular bicarbonate reabsorption and distal tubular acid secretion. The major compensatory mechanism in metabolic alkalosis is respiratory, since the presence of metabolic alkalosis implies renal dysfunction in either generating or failing to excrete increased amounts of bicarbonate. Hypoventilation is limited by the development of hypoxemia, which stimulates ventilation. Among the four major types of acid-base disorders, this compensatory mechanism is the least effective.