DISCUSSION: Beta agonist therapy has long been a standard therapeutic intervention for acute asthma exacerbations. In severe cases multiple beta agonist treatments may be required, increasing the potential of inducing a type B lactic acidosis[1,2]. The mechanism for the lactic acidosis is attributed to an increase in pyruvate production as well as inhibition of pyruvate oxidation leading to increased lactate production. Several reports have also attributed a component of the lactic acidosis to smooth muscle contraction and diaphragmatic fatigue. The increasing metabolic derangement results in worsening tachypnea as a compensatory mechanism. This creates a diagnostic challenge as tachypnea can be a sign of worsening asthma exacerbation potentially prompting clinicians to pursue further beta agonist therapy. Most of the cases reviewed demonstrated the development of lactic acidosis in patients who have received prolonged or multiple nebulized beta agonist treatments. The acidosis generally resolves within 24-48 hours, and in many cases within as little as 3 hours, of cessation of beta agonist therapy[1,2].