Opioid-induced Ventilatory Depression in Sleep Apnea: Reply

Our recent article on remifentanil in patients with obstructive sleep apnea concluded that “Obstructive sleep apnea status, apnea/hypopnea events per hour of sleep, or minimum nocturnal oxygen saturation measured by pulse oximetry did not influence the sensitivity to remifentanil-induced ventilatory depression in awake patients receiving a remifentanil infusion of 0.2 μg · kg^–1 of ideal body weight per minute.”¹  Our conclusion is supported by directly observed ventilation during remifentanil infusion, analyzed using published and validated models of remifentanil pharmacokinetics and the pharmacodynamic interaction between remifentanil and carbon dioxide on ventilation, and, as highlighted by the Editorial View by Henthorn and Olofsen,²  multiple analyses found that the absence of plasma concentration data did not significantly affect the estimate for the interindividual variability of the effect site concentration of remifentanil at which half-maximal ventilatory depression was observed, so it is unlikely our conclusion was affected. We agree with Overdyk et al. that our findings should not be extrapolated to other clinical scenarios where patients with obstructive sleep apnea may be at increased risk of opioid-induced ventilatory depression.

The authors declare no competing interests.