The most likely acid-base disorder in this patient is respiratory alkalosis with acute metabolic compensation. This patient has primary acute respiratory alkalosis, likely resulting from a panic attack associated with her anxiety disorder. Acute respiratory alkalosis is evidenced by a low PCO₂ and an appropriately reduced serum bicarbonate occurring in response to the lowered PCO₂. For each 10 mm Hg (1.3 kPa) decrease in PCO₂, serum bicarbonate falls acutely by 2.0 mEq/L (2.0 mmol/L) due to intracellular-to-extracellular shift of hydrogen ions as an immediate buffering mechanism. If the respiratory alkalosis is persistent, renal compensation will eventually occur, leading to reduced proximal tubule reabsorption of bicarbonate, and, after 24 to 48 hours, a further decrease in serum bicarbonate totaling 3.0 to 4.0 mEq/L (3.0-4.0 mmol/L) for every 10 mm Hg (1.3 kPa) decrease of PCO₂. The reduction in bicarbonate of 4.0 mEq/L (4.0 mmol/L) for the decrease in PCO₂ of 18 mm Hg (2.4 kPa) indicates that renal compensation has not yet occurred. The laboratory studies are not consistent with a primary metabolic alkalosis because the bicarbonate is not elevated.