Opioid Analgesics

Opioids relieve pain mainly by activating mu opioid receptors in the central and peripheral nervous systems. This reduces nociceptive transmission and changes the emotional response to pain. The same receptor activity can produce sedation, nausea, constipation, urinary retention, and respiratory depression. Respiratory depression is not an unpredictable allergic reaction. In the brainstem, mu-receptor activation blunts the normal ventilatory response to rising carbon dioxide. Breathing becomes slower and shallower, particularly after dose increases, rapid intravenous administration, or addition of another sedative. The patient may look comfortable while ventilation is failing. That mechanism gives the bedside priority: assess arousability and breathing, not just the pain score or oxygen saturation. Sedation commonly appears before clinically obvious respiratory depression. A patient who is increasingly difficult to rouse after an opioid needs immediate reassessment, even if the stated pain is improved and the pulse oximeter still reads normally. Full agonists such as morphine, hydromorphone, oxycodone, fentanyl, methadone, codeine, and tramadol have varying potency, onset, duration, metabolism, and interaction profiles. They are not interchangeable by milligram. Buprenorphine is different: it is a high-affinity partial mu agonist....