Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production

Background. In acute respiratory alkalosis, the severity of alkalaemiaisamelioratedbyadecreaseinplasma[HCO3 − ] of 0.2 mEq/L for each 1 mmHg decrease in PaCO2 .A lthough hyperventilation in panic disorder patients is frequently encountered in outpatients, the drop in plasma [HCO3 − ] sometimes surpasses the expectation calculated from the above formula. The quantitative relationship between reduced PaCO2 and plasma [HCO3 − ] in acute respiratory alkalosis has not been studied in panic disorder patients. Our objective was to provide reference data for the compensatory metabolic changes in acute respiratory alkalosis in panic disorder patients. Methods. In 34 panic disorder patients with hyperventilation attacks, we measured arterial pH, PaCO2 ,p lasma [HCO3 − ] and lactate on arrival at the emergency room. Results. For each decrease of 1 mmHg in PaCO2 ,p lasma [HCO3 − ] decreased by 0.41 mEq/L. During hypocapnia, panic disorder patients exhibited larger increases in serum lactate levels (mean ± SD; 2.59 ± 1.50 mmol/L, range; 0.78–7.78 mmol/L) than previously reported in non-panic disorder subjects. Plasma lactate accumulation was correlated with PaCO2 (P < 0.001). Conclusions. These results suggest that the compensatory metabolic response to acute respiratory alkalosis is exaggerated by increased lactic acid production in panic disorder patients. Here, we call attention to the diagnosis of acid–base derangements by means of plasma [HCO3 − ] and lactate concentration in panic disorder patients.