. if a previously effective dosage regimen fails to provide the usual relief, medical advice should be sought immediately, as this is often a sign of seriously worsening asthma that would require reassessment of therapy.

lude mild reactions. *the finding of no arrhythmias and no palpitations after albuterol administration in the clinical study should not be interpreted as indicating that these adverse effects cannot occur after the administration of inhaled albuterol. +in most cases of bronchospasm, this term was generally used to describe exacerbations in the underlying pulmonary disease. cases of urticaria, angioedema, rash, bronchospasm, hoarseness, oropharyngeal edema, arrhythmias (including atrial fibrillations, supraventricular tachycardia, extrasystoles) have been reported after the use of albuterol sulfate inhalation solution. adverse

tudies and other clinical experience have shown that inhaled albuterol, like other beta-adrenergic agonist drugs, can produce a significant cardiovascular effect in some patients, as measured by pulse rate, blood pressure, symptoms, and/or electrocardiographic changes. albuterol is longer acting than isoproterenol in most patients by any route of administration because it is not a substrate for the cellular uptake processes for catecholamines nor for catechol- o-methyl transferase. studies in asthmatic patients have shown that less than 20% of a single albuterol dose was absorbed following either ippb (intermittent positive-pressure breathing) or nebulizer administration; the remaining amount was recovered from the nebulizer and apparatus and expired air. most of the absorbed dose was recovered in the urine 24 hours after drug administration. following a 3 mg dose of nebulized albuterol, the maximum albuterol plasma level at 0.5 hours was 2.1 ng/ml (range, 1.4 to 3.2 ng/ml). there was a significant dose-related response in fev 1 (forced expiratory volume in one second) and peak flow rate. it has been demonstrated that following oral administration of 4 mg of albuterol, the elimination half-life was five to six hours. animal studies show that albuterol does not pass the blood-brain barrier. recent studies in laboratory animals (minipigs, rodents, and dogs) recorded the occurrence of cardiac arrhythmias and sudden death (with histologic evidence of myocardial necrosis) when beta-agonists and methylxanthines were administered concurrently. the significance of these findings when applied to humans is currently unknown. in controlled clinical trials, most patients exhibited an onset of improvement in pulmonary function within 5 minutes as determined by fev 1. fev 1 measurements also showed that the maximum average improvement in pulmonary function usually occurred at approximately 1 hour following inhalation of 2.5 mg of albuterol by compressor-nebulizer and remained close to peak for 2 hours. clinically significant improvement in pulmonary function (defined as maintenance of a 15% or more increase in fev 1 over baseline values) continued for 3 to 4 hours in most patients and in some patients continued up to 6 hours. in repetitive dose studies, continued effectiveness was demonstrated throughout the three-month period of treatment in some patients. published reports of trials in asthmatic children aged 3 years or older have demonstrated significant improvement in either fev 1 or pefr within 2 to 20 minutes following a single dose of albuterol inhalation solution. an increase of 15% or more in baseline fev 1 has been observed in children aged 5 to 11 years up to 6 hours after treatment with doses of 0.10 mg/kg or higher of albuterol inhalation solution. single doses of 3, 4, or 10 mg resulted in improvement in baseline pefr that was comparable in extent and duration to a 2 mg dose, but doses above 3 mg were associated with heart rate increases of more than 10%.