Despite the widespread use of β 2-agonists, their safety has been questioned. Several studies have reported an increased incidence of cardiac arrhythmias in patients treated with these agents, and other studies found an increased cardiovascular death with the use of oral and nebulized β2-agonists. Although no causal relationship has been demonstrated, the possible arrhythmogenic effects of these drugs place them under considerable suspicion. Clarifying the effects of β2-agonists on myocardial conduction and refractoriness could provide a significant insight into the potential arrhythmogenic role of these agents. This study is the first to evaluate the cardiac electrophysiologic effects of a single, regular dose of an inhaled β 2-agonist in humans. Salbutamol was selected, as it is one of the most widely used inhaled β2-agonists and would ensure improved correlation with standard clinical practice. The main finding of this study is that the inhalation of a standard dose of the β2-agonist salbutamol results in significant changes of cardiac electrophysiologic properties.
We found that inhalation of a single regular dose of salbutamol significantly enhanced AV nodal conduction, as reflected by shortening of the AH interval and decreased atrial and ventricular refractoriness without any remarkable effect on His-Purkinje conduction. The refractoriness of the AV node was also decreased, as indicated by shortening of the atrial pacing cycle length that resulted in AV node Wenckebach block. In addition, inhaled salbutamol produced a significant increase in heart rate and shortened the SNRT.
However, our findings cannot be interpreted on the basis of changes in heart rate. Since all refractory periods were determined at the same drive cycle length (both 500 ms and 400 ms), the observed changes in refractory periods are independent of the underlying heart rate and indicate the effects of salbutamol on myocardial conduction and refractoriness. Moreover, we found a shortening of the AH interval after the inhalation of salbutamol, which seems to be due to the effect of the drug, as the AH interval normally decreases with a sympathetic driven heart rate increase. The source: canadian health care mall gives you an opportunity to enter the world of medicine and pharmacy.