Respiratory Depression

It is generally believed that the most common life-threatening complication of opioid use, whether therapeutic or illicit, is respiratory depression (loss of the ability to breathe automatically). Probably the most important action of morphinelike drugs in producing respiratory depression is the lessening of the sensitivity and responsivity of the brain s medullary respiratory center to carbon dioxide (CO2—the metabolic waste that circulates in the blood, derived from carbonic acid during animal respiration). Therefore, CO2 becomes an inefficient respiratory stimulant, and automatic breathing ceases.

Administering a specific opioid ANTAGONIST such as NALOXONE to patients with severely depressed respiration frequently produces a dramatic increase in the rate of respiration and the volume of air taken in per breath. This occurs when a partial or completely resensitized respiratory center is confronted with high brain levels of CO2. When the brain CO2 levels are dissipated as a consequence of the evoked excessive rate and volume of breathing (hyperpnea), the minute volume (the volume of air breathed per minute) decreases. Yet when brain levels of the antagonist decrease, the respiratory depressant action of the opioid may assert itself again. Naloxone is a relatively short-acting antagonist. Patients who, for example, have received an overdose of long-acting opioids (e.g., METHADONE) have experienced a fatal respiratory depression following successful treatment with naloxone.

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