Key result
Inhalation of 0.2 mg salbutamol in healthy subjects significantly increased cardiac output to 7.7 L/min (P<0.05) and shifted sympathovagal balance towards increased sympathetic tone.
Why the study?
Does inhaled salbutamol alter haemodynamic parameters and cardiovascular autonomic control in healthy subjects?
RCT (n=12)
single-blinded
randomized
Does inhaled salbutamol alter haemodynamic parameters and cardiovascular autonomic control in healthy subjects?
p-value: p=<0.05
Inhaled salbutamol at therapeutic doses induces significant short-term haemodynamic changes and increases sympathetic autonomic tone in healthy subjects, providing a potential mechanism for associated cardiac risks.
May warrant caution in cardiac patients; extends RCT evidence of beta-agonist effects to sympathovagal balance.
WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Previous reports have demonstrated a link between inhaled β 2 ‐agonist use and cardiovascular morbidity and mortality. • The underlying mechanism for this relationship, however, remains controversial. WHAT THIS STUDY ADDS • Inhalation of a therapeutic dose of salbutamol resulted in significant haemodynamic changes, which were accompanied by a shift in cardiovascular autonomic tone towards increased sympathetic outflow in the absence of baroreceptor activation. • The observed changes in cardiac autonomic function may contribute to an increased cardiac risk associated with inhaled β 2 ‐agonist treatment. AIMS To investigate short‐term effects of inhaled salbutamol on haemodynamic changes and cardiovascular autonomic control. METHODS A randomized, single‐blinded, placebo‐controlled study of 0.2 mg of inhaled salbutamol was conducted on 12 healthy nonsmoking volunteers with a mean age of 24 ± 2 years at two different testing sessions. Non‐invasively obtained continuous haemodynamic measurements of cardiac output, beat‐to‐beat arterial blood pressure, and total peripheral resistance were recorded prior to and for a total of 120 min after inhalation of the respective study drug. Continuous cardiovascular autonomic tone was recorded using power spectral analysis of heart rate and blood pressure variability. Spontaneous baroreceptor activity was assessed by the sequence method. RESULTS There were no significant changes in any of the baseline parameters between the different testing sessions. Inhalation of salbutamol caused a significant increase in cardiac output from 6.7 ± 1.3 to 7.7 ± 1.4 l min −1 ( P < 0.05), and a decrease in total peripheral resistance from 1076 ± 192 to 905 ± 172 dyne s −1 cm −5 ( P < 0.05) within 15 min after inhalation. Moreover, salbutamol significantly increased sympathetically mediated low‐frequency heart rate variability ( P < 0.01), whereas parasympathetically mediated high‐frequency heart rate variability decreased ( P < 0.01). All changes persisted for approximately 30 min and were fully reversible at 120 min. There were no significant changes in systolic blood pressure variability or spontaneous baroreceptor activity. CONCLUSIONS Inhalation of therapeutic doses of salbutamol in healthy subjects resulted in significant haemodynamic changes and a shift of sympathovagal balance towards increased sympathetic tone in the absence of baroreceptor activation.
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Cekici et al. (2009) conducted an RCT in Healthy subjects (n=12). salbutamol vs. placebo was evaluated on cardiac output (l min-1) (p=<0.05). Inhalation of 0.2 mg salbutamol in healthy subjects significantly increased cardiac output to 7.7 L/min (P<0.05) and shifted sympathovagal balance towards increased sympathetic tone.
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