Study objectives were to evaluate the 1-hour decision point for discharge or admission for acute asthma; to compare this decision point to the admission recommendations of the Expert Panel Report 2 (EPR-2) guidelines; to develop a model for predicting need for admission in acute asthma. The design used was a prospective preinterventional and postinterventional comparison. The setting was a university hospital emergency department. Participants included 50 patients seeking care for acute asthma. Patients received standard therapy and were randomized to receive albuterol by nebulizer or metered-dose inhaler with spacer every 20 minutes up to 2 hours. Symptoms, physical examination, spirometry, pulsus paradoxus, medication use, and outcome were evaluated. Based on clinical judgment, the attending physician decided to admit or discharge after 1 hour of therapy. Outcome was compared to the EPR-2 guidelines. Post hoc statistical analyses examined predictors of the need for admission from which a prediction model was developed. Maximal accuracy of the admit versus discharge decision occurred at 1 hour of therapy. Using FEV(1) alone as an outcome predictor yielded suboptimal performance. FEV(1) at 1 hour plus ability to lie flat without dyspnea were the best indicators of response and outcome. A model predictive of the need for admission was developed. It performed better (P =.0054) than the admission algorithm of the EPR-2 guidelines. The decision to admit or discharge acute asthmatics from the ED can be made at 1 hour of therapy. No absolute value of peak flow or FEV(1) reliably predicts need for hospital admission. The EPR-2 guideline thresholds for admission are barely adequate as outcome predictors. A clinical model is proposed that may allow more accurate outcome prediction.

The beta(2)-adrenergic agonist, albuterol, is used as a bronchodilator by patients with asthma and consists of a racemic mixture of (R)- and (S)-albuterol. However, the action of the individual enantiomers is poorly understood. Consequently, we investigated the effects of (R)-, (S)- and racemic-albuterol on airway smooth muscle cell (SMC) contraction and Ca(2+) signaling in mouse lung slices with phase-contrast and confocal microscopy. (R)-albuterol relaxed airways contracted with methacholine (MCh) in a dose-dependent manner. By contrast, (S)-albuterol had no effect on airways. (R)-albuterol had a greater relaxant effect than a double concentration of racemic albuterol. Because MCh-induced contraction of airway SMCs is mediated by Ca(2+) oscillations and an increase in Ca(2+) sensitivity, the effects of albuterol on these responses were examined. Both (R)- and racemic albuterol decreased the frequency of the MCh-induced Ca(2+) oscillations by a similar amount. However, (R)-albuterol was more effective than racemic albuterol in decreasing the Ca(2+) sensitivity of the airway SMCs in "model" lung slices with a clamped [Ca(2+)](i). In contrast, (S)-albuterol had no effect on the Ca(2+) oscillations or the Ca(2+) sensitivity. In conclusion, (R)-albuterol consistently induced a greater airway relaxation than racemic albuterol, and (S)-albuterol appears to be responsible for this reduced efficacy.