Lactic acidosis is a marker of tissue hypoperfusion and impairs oxygen delivery. High lactate levels are associated with altered systemic hemodynamics, tissue hypoperfusion, and altered cellular metabolism. Increased lactate levels have also been reported as a complication of β-adrenergic agents administered during asthma therapy. A 49-year-old woman with a prior diagnosis of asthma presented to the emergency department in respiratory distress. She immediately received, in 2 hours, 4 bronchodilator aerosols (ipratropium bromide 0.5 mg/2 mL and terbutaline 5 mg/2 mL) and methylprednisolone intravenous (120 mg). After these 4 aerosols, she was still dyspneic. First, arterial blood gases (pH 7.38; PCO2, 3.92 kPa; HCO3, 19.2 mmol/L) and arterial lactate (lactate, 7.96 mmol/L) were performed with a second series of 4 aerosols. Second, arterial blood gases (pH 7.29; PCO2, 4.01 kPa; HCO3, 15.4 mmol/L) and arterial lactate (lactate, 10.47 mmol/L) were performed at the end of the second series of aerosols. There was no hypoxemia, no inadequate cardiac output state, no anemia, no sepsis, and no use of biguanides. Previous studies have suggested that administration of β agonists can lead to lactic acidemia in the absence of hypoxia or shock, but it is the highest level of lactate that we found in the literature. In sepsis and shock, lactic acidosis is used as a marker of disease severity. In this case, it is not necessarily the sign of an immediate gravity.