Tramadol is a centrally acting opioid with a low affinity for mu-opioi
d receptors, which has been claimed not to depress respiration as do t
he classic opioids. The respiratory effects of intravenous (i.v.) peth
idine (0.6 mg kg(-1)) and tramadol (0.6 mg kg(-1)) were com pared in 3
6 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 breat
hed halothane in 70% nitrous oxide and oxygen via a non-rebreathing va
lve. Inspiratory and expiratory oxygen, and end-tidal carbon dioxide c
oncentrations (PETCO2), tidal volume (V-T), minute volume of ventilati
on (MV) and respiratory rate were monitored by a side-stream spirometr
y at an end-tidal halothane of 0.3%. The recordings were collected bef
ore 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 w
as 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.