Lactic acidosis has diverse causes and is usually classified as Type A, which is associated with poor tissue perfusion and/or hypoxemia, or as Type B, which has multiple causes but no tissue hypoperfusion (Table 1). Patients with asthma may develop acute metabolic acidosis secondary to Type A causes such as shock, sepsis, or refractory hypoxemia or secondary to Type B causes. Our patient had a normal BP and adequate oxygenation, and Type B causes seem more likely. Patients with severe asthma have increased respiratory work, and high metabolic demands are placed on their respiratory muscles. Several studies have reported high creatine kinase levels in people with asthma and acute respiratory distress, and this presumably represents respiratory muscle injury. Failure to meet a high level of oxygen demand causes tissue hypoxia and subsequent production of lactic acid and could explain lactic acidosis in some patients. However, lactate production increases in well-oxygenated skeletal muscles during exercise, and some studies suggest that there is a poor correlation between oxygen saturation of muscle myoglobin and measured lactate concentration. Thus, net intracellular production of lactate may occur in either hypoxic or normoxic conditions in respiratory muscles in patients with severe asthma. The lactic acidosis in these patients could also reflect a hyperadrenergic state with excess catecholamines. Catecholamines can have an exogenous origin secondary to therapy or an endogenous origin secondary to severe stress and anxiety. Lactic acidosis has been associated with epinephrine (subcutaneous), albuterol (inhaled and IV), and terbutaline (subcutaneous). Increased catecholamine levels stimulate glycolysis and glycogenolysis, which subsequently increases pyruvate generation and its conversion to lactate. Thus, acute acidemia can develop with exogenous β-agonist therapy; this likely occurred in our patient, especially because she used large amounts of epinephrine prior to hospitalization, and this catecholamine has greater effects on carbohydrate metabolism. Concomitant steroid use enhances β2-receptor sensitivity and could promote the production of lactic acid. Patients with catecholamine excess are also at risk for hypokalemia, hypophosphatemia, and hyperglycemia.