Oxycodone is a pure agonist opioid whose principal therapeutic action is analgesia. Other
members of the class known as opioid agonists include substances such as morphine,
hydromorphone, fentanyl, codeine, and hydrocodone. Pharmacological effects of opioid
agonists include anxiolysis, euphoria, feelings of relaxation, respiratory depression,
constipation, miosis, and cough suppression, as well as analgesia. Like all pure opioid
agonist analgesics, with increasing doses there is increasing analgesia, unlike with mixed
agonist/antagonists or non-opioid analgesics, where there is a limit to the analgesic effect
with increasing doses. With pure opioid agonist analgesics, there is no defined maximum
dose; the ceiling to analgesic effectiveness is imposed only by side effects, the more serious
of which may include somnolence and respiratory depression.
Central Nervous System
The precise mechanism of the analgesic action is unknown. However, specific CNS opioid
receptors for endogenous compounds with opioid-like activity have been identified
throughout the brain and spinal cord and play a role in the analgesic effects of this drug.
Oxycodone produces respiratory depression by direct action on brain stem respiratory
centers. The respiratory depression involves both a reduction in the responsiveness of the
brain stem respiratory centers to increases in carbon dioxide tension and to electrical
Oxycodone depresses the cough reflex by direct effect on the cough center in the medulla.
Antitussive effects may occur with doses lower than those usually required for analgesia.
Oxycodone causes miosis, even in total darkness. Pinpoint pupils are a sign of opioid
overdose but are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origin
may produce similar findings). Marked mydriasis rather than miosis may be seen with
hypoxia in the setting of OxyContin® overdose