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The respiratory-depressant actions of opioids represent their most serious adverse effect. Although significant adverse events related to opioid-induced respiratory depression are presumably preventable, they persist with a perioperative incidence of approximately 0.1% to 1%, no matter what the route of administration. [152]
Morphine has been shown to have a depressant effect on mucociliary flow in the trachea, which is one of the most important defenses against respiratory tract infections.[153] On the other hand, morphine had no effect on nasal cilia beating frequency in vitro.[154] Morphine may have an effect on cilia in vivo because of effects on neural connections that are absent from in vitro preparations.
Opioids, by decreasing both pain and central ventilatory drive, are effective agents in preventing hyperventilation induced by pain or anxiety.[155] [156] The lack of adequate pain relief can also cause postoperative respiratory dysfunction. Opioids can be used as postoperative analgesics to prevent respiratory dysfunction. The antitussive actions of opioids are well known and central in origin. However, fentanyl, sufentanil, and alfentanil curiously elicit a brief cough in up to 50% of patients when injected by intravenous bolus.[157]
Opioids are excellent agents for depressing upper airway, tracheal, and lower respiratory tract reflexes, but the mechanism is not clear. Although opioids can affect the contractile responses of airway smooth muscles, the clinical significance and relevance of opioid-induced effects on airway resistance remains controversial. [158] Opioids blunt or eliminate somatic and autonomic responses to tracheal intubation, allowing patients to tolerate endotracheal tubes without coughing or "bucking." Opioids can also help to avoid increases in bronchomotor tone in asthma. Fentanyl has antimuscarinic, antihistaminergic, and anti-serotoninergic actions and may be more effective than morphine in patients with asthma or other bronchospastic diseases. The relatively slight impact of opioids on hypoxic pulmonary vasoconstriction contributes to their minimal interference with pulmonary gas exchange.
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