Measurement of this patient's urine chloride level is the most appropriate next step in management. She has a metabolic alkalosis as evidenced by the elevated blood pH and elevated serum bicarbonate level. Metabolic alkalosis is caused by net loss of acid or retention of serum bicarbonate. Metabolic alkalosis can be classified as either occurring with normal extracellular fluid volume, hypovolemia, or decreased effective arterial blood volume and increased extracellular fluid volume (heart failure, cirrhosis, nephrosis), or occurring with increased extracellular fluid volume and hypertension. This patient's clinical volume status is equivocal; blood pressure is slightly low and pulse rate is slightly high, yet there is peripheral edema, which could be explained by either cardiac or noncardiac causes (for example, a side effect of amlodipine), and mild hypoxia, which could be cardiac or pulmonary in etiology, given her medical history. Urine chloride measurement can help determine the cause of metabolic alkalosis, particularly if it is difficult to clinically assess volume status. In such patients, a low (<15 mEq/L [15 mmol/L]) urine chloride suggests reduction in extracellular volume and the presence of saline-responsive metabolic alkalosis. Conditions that are associated with saline-responsive metabolic alkalosis include vomiting, remote use of diuretics, and post-hypercapnic metabolic alkalosis. If the urine chloride is high (>15 mEq/L [15 mmol/L]), the metabolic alkalosis is saline resistant and can be caused by active diuretic use, stimulant laxative abuse, and rare renal tubular disorders such as Gitelman and Bartter syndromes. In this case, the patient's metabolic alkalosis is due to vomiting, and a low urine chloride would direct appropriate management to saline infusion.

Saline infusion without first categorizing the nature of the metabolic alkalosis is inappropriate and potentially dangerous in patients with limited cardiac reserve or hypoxia.

There is no clear evidence of volume overload that requires administration of a loop diuretic such as furosemide. Loop diuretic therapy is likely to worsen metabolic alkalosis by increasing the secretion of aldosterone and distal delivery of sodium, resulting in urine potassium and hydrogen loss.

In patients with metabolic alkalosis, measurement of urine chloride rather than urine sodium is used to determine volume status and saline responsiveness because urine sodium can be artificially high during periods of appropriate compensatory urine bicarbonate excretion (sodium is the primary cation excreted in an obligatory fashion with bicarbonate).