Opioid Safety and Monitoring

Opioids reduce pain mainly by activating mu receptors in the central and peripheral nervous systems. That receptor activity dampens pain transmission, but it also suppresses the brainstem response to rising carbon dioxide. The same medication that makes pain tolerable can therefore make breathing slower, shallower, or absent. Mu-receptor activation also commonly causes drowsiness, nausea, constipation, urinary retention, reduced cough, and sometimes hypotension. Respiratory depression is the dangerous adverse effect because it can progress from reduced arousability to hypoventilation and cardiac arrest. Risk rises after a first dose, dose increase, rapid intravenous administration, or the addition of another sedating medication. Older adults, opioid-naive patients, and people with sleep-disordered breathing, chronic lung disease, hypoxia, renal impairment, or hepatic impairment have less physiologic reserve. Alcohol, benzodiazepines, sedating antihistamines, gabapentinoids, and other central nervous system depressants can compound the effect. A patient may still report severe pain while becoming dangerously sedated. Pain intensity does not cancel the respiratory assessment. An experienced nurse looks first at arousability, respiratory effort, and the trend in oxygen requirement—not only at the number the patient gives for pain.