This patient has metabolic alkalosis as implied by the elevated serum bicarbonate and is hypovolemic as evidenced by the orthostatic blood pressure and pulse changes. Such a patient would be expected to have low urine concentrations of sodium and chloride. However, these patient’s urine electrolytes show increased excretion of sodium and chloride despite the evident hypovolemia. These findings suggest the presence of active diuretic use or a renal tubular defect that impairs handling of sodium and chloride, such as Bartter and Gitelman syndromes.