Acute electrophysiologic effects of inhaled salbutamol in humans.
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.
Kallergis
Eleftherios M
EM
Department of Cardiology, University Hospital of Heraklion, 71000, Voutes, Heraklion-Crete, Greece.
Manios
Emmanuel G
EG
Kanoupakis
Emmanuel M
EM
Schiza
Sophia E
SE
Mavrakis
Hercules E
HE
Klapsinos
Nikolaos K
NK
Vardas
Panos E
PE
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
D000318:Adrenergic beta-Agonists; D000420:Albuterol