Tramadol is a centrally acting opioid with a low affinity resfor μ-opioid receptors, which has been claimed not to depress respiration as do the classic opioids. The respiratory effects of intravenous (i.v.) pethidine (0.6 mg kg−1) and tramadol (0.6 mg kg−1) were compared in 36 ASA Grade I–II patients in a placebo-controlled double-blind study. After induction of anaesthesia with propofol followed by suxamethonium-facilitated endotracheal intubation, the patients spontaneously breathed halothane in 70% nitrous oxide and oxygen via a non-rebreathing valve. Inspiratory and expiratory oxygen, and end-tidal carbon dioxide concentrations (PetCO2), tidal volume (VT), minute volume of ventilation (MV) and respiratory rate were monitored by a side-stream spirometry at an end-tidal halothane of 0.3%. The recordings were collected before surgery. Pethidine caused significant respiratory depression seen as an increase in fractional inspiratory–expiratory oxygen difference and PetCO2 and as a decrease in MV and respiratory rate. However, the effects of tramadol were similar to those of a placebo. Tidal volume was not affected by any study drug. In conclusion, tramadol 0.6 mg kg−1 was shown not to be associated with respiratory depression, unlike equipotent dose of pethidine in this setting.