Introduction: Opioid respiratory effects have been studied in healthy volunteers or post-operative patients. Pain appears to counter the respiratory suppressive effects of mu agonists on the medullary respiratory center. Diminished responsiveness to CO2 will lead to elevated Pco2 which may predate reduced respiratory rate. We studied respiratory function, end-tidal CO2 (eTCO2) and O2 sats in patients on opioids for pain.
Study method: Palliative in-patients were screened for eligibility. Vitals, RR, a 10 point numerical scale (NRS) for rest dyspnea, MRC scale O2 sat, eTCO2 and spirometry were measured. Pain was assessed by NRS and cognition by Bedside Confusion Scale. Arterial blood gases were obtained if eTCO2 exceeded 50 mm Hg x 2 at 30 minutes intervals. Cancer patients with pain, cognitively intact and not requiring oxygen were placed on trial after informed consent. An eTCO2, O2 Sat, RR and Delirium Scale were obtained daily until pain control. Pain control was NRS<4 and 4 or less daily rescue doses. Spirometry was done at the end of study.
Results: Eighteen of 68 patients admitted to the palliative service for pain control were eligible and completed the study. Seven were females, mean age was 60 (range 39-85 years). Five had mixed, 5 visceral and 8 somatic pain. Cancer distribution was similar to the unit’s demographics. Opioids were morphine in fifteen, fentanyl in two and hydromorphine in one. Respiratory rate transiently dropped in one patient to 9, otherwise RRwas > 12. O2 sats were consistently > 92% in all patients and eTCO2 was < 50 in all patients during study. The highest eTCO2 was 44. Three had > 4 mm Hg change in eTCO2, two had a - 9 mm Hg and one + 10 mm Hg change.
Conclusions: Titration of opioids to analgesia is not associated with respiratory depression in advanced cancer.