title: Acute electrophysiologic effects of inhaled salbutamol in humans.
abstract: OBJECTIVE
  Although inhaled beta2-agonists are in widespread use, several reports question their potential arrhythmogenic effects. The purpose of this study was to evaluate the cardiac electrophysiologic effects of a single, regular dose of an inhaled beta2-agonist in humans.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Tertiary referral center.
  
  
  METHODS
  Six patients with bronchial asthma and 12 patients with mild COPD.
  
  
  METHODS
  All patients underwent an electrophysiologic study before and after the administration of salbutamol solution (5 mg in a single dose).
  
  
  RESULTS
  Sinus cycle length, sinus node recovery time (SNRT), interval from the earliest reproducible rapid deflection of the atrial electrogram in the His bundle recording to the onset of the His deflection (AH), interval from the His deflection to the onset of ventricular depolarization (HV), Wenckebach cycle length (WCL), atrial effective refractory period (AERP), and ventricular effective refractory period (VERP) were evaluated just before and 30 min after the scheduled intervention. Salbutamol, a selective beta2-agonist, administered by nebulizer had significant electrophysiologic effects on the atrium, nodes, and ventricle. The AH length decreased from 86.1 +/- 19.5 ms at baseline to 78.8 +/- 18.4 ms (p < 0.001), and the WCL decreased from 354.4 +/- 44.2 to 336.6 +/- 41.7 ms (p = 0.001). Salbutamol significantly decreased the AERP and VERP too while leaving the HV unchanged. Additionally, inhaled salbutamol increased heart rate (from 75.5 +/- 12.8 beats/min at baseline to 93.1 +/- 16 beats/min, p < 0.001) and shortened the SNRT (from 1,073.5 +/- 178.7 to 925.2 +/- 204.9 ms, p = 0.001).
  
  
  CONCLUSIONS
  Inhaled salbutamol results in significant changes of cardiac electrophysiologic properties. Salbutamol enhances atrioventricular (AV) nodal conduction and decreases AV nodal, atrial, and ventricular refractoriness in addition to its positive chronotropic effects. These alterations could contribute to the generation of spontaneous arrhythmias.
authors.affiliation: Department of Cardiology, University Hospital of Heraklion, 71000, Voutes, Heraklion-Crete, Greece.
authors.forename: Eleftherios M
authors.initials: EM
authors.lastname: Kallergis
authors.forename: Emmanuel G
authors.initials: EG
authors.lastname: Manios
authors.forename: Emmanuel M
authors.initials: EM
authors.lastname: Kanoupakis
authors.forename: Sophia E
authors.initials: SE
authors.lastname: Schiza
authors.forename: Hercules E
authors.initials: HE
authors.lastname: Mavrakis
authors.forename: Nikolaos K
authors.initials: NK
authors.lastname: Klapsinos
authors.forename: Panos E
authors.initials: PE
authors.lastname: Vardas
mesh_terms: D000280:Administration, Inhalation; D000318:Adrenergic beta-Agonists / Q000009:adverse effects* / Q000627:therapeutic use; D000420:Albuterol / Q000009:adverse effects* / Q000627:therapeutic use; D001249:Asthma / Q000175:diagnosis / Q000188:drug therapy; D001283:Atrioventricular Node / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000188:drug therapy; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D016277:Ventricular Function, Left / Q000187:drug effects; D016278:Ventricular Function, Right / Q000187:drug effects
chemical_list: D000318:Adrenergic beta-Agonists; D000420:Albuterol