Abstract

Opioids are widely used for the clinical management of acute and chronic pain. Opioids disrupt the temporal organization of sleep with reduced sleep efficiency, increased time for sleep onset, and reduced stage 3 non–rapid eye movement sleep and rapid eye movement sleep. Such sleep disruption can decrease pain thresholds and promote hyperalgesia counterproductively, even in pain-free individuals. Opioids also blunt wakefulness and can produce dose-dependent states of torpor. Further, they depress the ventilatory responses to hypercarbia and hypoxia, predisposing to hypoventilation, increasing upper airway resistance, and depressing arousal responses. Opioid-induced respiratory depression can be synergistic with comorbid conditions commonly encountered in sleep medicine, such as obstructive sleep apnea and sleep-related hypoventilation. Increased vigilance on the part of health care providers is indicated when opioids are part of a treatment plan for obese patients and for patients with preexisting sleep disorders. Furthermore, chronic opioid use is frequently associated with the occurrence of central sleep apnea. In geriatric and pediatric patients, age-specific pharmacokinetics can enhance opioid potency and decrease opioid elimination. The challenge for clinicians when considering prescribing opioids is to achieve adequate analgesia while minimizing respiratory depression, blunting of wakefulness, sleep disruption, drug tolerance, and potential for addiction.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call