The administration of rapacuronium increases the risk of severe bronchospasm. There have been no studies of pulmonary function directly demonstrating airway constriction with rapacuronium in children. In this study, 10 ASA physical status I or II patients (aged 2-6 yr) were randomly divided into 2 equal groups, receiving either rapacuronium or mivacurium. Anesthesia was induced with sevoflurane and maintained with remifentanil (0.2-0.3 microg. kg(-1). min(-1)) and propofol (200-250 microg. kg(-1). min(-1)) infusions. We performed three sets of pulmonary function tests: baseline, after the administration of muscle relaxant, and after the administration of a beta(2) agonist. In both groups, there were no changes in static respiratory compliance. The increase in total respiratory system resistance after the administration of rapacuronium did not reach statistical significance (214.4% +/- 122.65% of baseline, P approximately 0.1), whereas maximal expiratory flow at 10% of forced vital capacity (MEF)(10) and MEF(functional residual capacity) on partial flow-volume curves by the forced deflation technique decreased markedly (53.4% +/- 18.49%, P < 0.01 and 41.3% +/- 27.42%, P < 0.001, respectively). With the administration of mivacurium, no changes were observed in respiratory system resistance (109.5% +/- 30.28%). MEF(10) decreased slightly (77.0% +/- 9.03%, P < 0.005) whereas MEF(FRC) did not (81.2% +/- 29.85%, not significant). After the administration of a beta(2) agonist, all measurements returned to baseline. Thus, the administration of rapacuronium consistently results in lower airway obstruction with minimal changes in static respiratory compliance when compared with mivacurium.
Implications: Pulmonary function tests in the present study showed that rapacuronium consistently causes severe bronchoconstriction, confirming clinical case reports of bronchospasm. The bronchoconstriction is reversible with albuterol. Mivacurium also causes very mild subclinical bronchoconstriction.