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This patient's arterial pH >7.45 is consistent with alkalemia.  The PaCO₂ is elevated (>40 mm Hg), indicating a respiratory acidosis, which does not explain the alkalemia.  Therefore, primary metabolic alkalosis with respiratory compensation is most likely present.  When the etiology of metabolic alkalosis is unknown, assessment of volume status and measurement of urine chloride can be helpful.

Because low Cl^- impairs renal excretion of HCO₃^-, total body chloride depletion often plays an important role in the pathogenesis of metabolic alkalosis.  Etiologies of metabolic alkalosis that involve temporary chloride depletion (hypovolemia) will demonstrate low urine chloride and are amenable to treatment with Cl^- repletion (saline responsive).  These etiologies include:

• Nasogastric suctioning or severe vomiting, which involve loss of H⁺ and Cl^- (ie, hydrochloric acid) from the stomach.
• Loop or thiazide diuretic overuse, which involve loss of Cl^- and retention of HCO₃^- by the kidneys.  Of note, urine chloride will be high with recent use but drops to low levels once the diuretic effect wanes.

Metabolic alkalosis can also occur in the absence of significant chloride depletion.  Conditions of mineralocorticoid excess (eg, primary hyperaldosteronism) cause metabolic alkalosis primarily due to aldosterone-mediated H⁺ loss from the kidneys.  These patients have hypervolemia (eg, hypertension), resulting in a pressure natriuresis with high urine chloride levels; the metabolic alkalosis does not correct with Cl^- repletion (saline unresponsive) due to the persistent mineralocorticoid effect.

Certain renal tubular channelopathies (eg, Bartter and Gitelman syndromes) represent a special case.  Although affected patients are hypovolemic and total body chloride is low, high urine chloride is present because the defect persistently impairs renal Cl- reabsorption.

(Choices A and E)  Assessment of serum ketones and urine glucose is helpful in the evaluation of diabetic ketoacidosis as a cause of metabolic acidosis.  However, this patient has metabolic alkalosis.

(Choices B and C)  Intravascular volume depletion can also contribute to metabolic alkalosis by increasing renal bicarbonate reabsorption.  However, serum sodium concentration is an indication of the relative amounts of total body sodium and total body water; it provides little information about overall volume status (ie, hypo- or hypernatremia can occur with hypovolemia, euvolemia, or hypervolemia).  Serum osmolality usually reflects serum sodium concentration unless high levels of other osmotically active substances are present (eg, glucose, ethanol); like serum sodium, it cannot be used to reliably differentiate hypovolemia from hypervolemia.

Educational objective:
Total body chloride depletion is often important in the pathophysiology of metabolic alkalosis.  Measurement of urine chloride can be helpful in determining the underlying etiology.