## Why "Intravenous naloxone bolus followed by infusion if needed, as it competitively antagonizes the μ receptor" is right Naloxone is a competitive μ-receptor antagonist and the first-line agent for opioid overdose reversal. The clinical presentation (pinpoint pupils, respiratory depression, coma) is pathognomonic for μ-receptor activation. Naloxone rapidly reverses all μ-mediated effects including respiratory depression. Critically, naloxone has a short half-life (30–90 minutes) compared to longer-acting opioids like heroin's active metabolites and especially methadone (24–36 hours), necessitating repeated dosing or continuous infusion to prevent re-sedation and recurrent respiratory depression. (KD Tripathi 9e, Ch 34) ## Why each distractor is wrong - **Intravenous naltrexone as a single dose, which has longer duration than naloxone**: While naltrexone is also a μ-antagonist, it has a LONGER half-life (4–10 hours), making it unsuitable for acute overdose management where rapid onset and titratability are essential. Naloxone is the standard of care for acute reversal. - **Mechanical ventilation alone until the opioid is metabolized**: This is supportive care only and does not address the underlying receptor blockade. It delays definitive treatment and risks prolonged respiratory support. Naloxone reversal is far superior and allows spontaneous breathing restoration. - **Subcutaneous morphine to compete for the same receptor and displace heroin**: This is dangerous and contradictory—adding another μ agonist would worsen respiratory depression and coma, not reverse it. Competitive antagonism (naloxone), not agonism, is required. **High-Yield:** Naloxone = competitive μ-antagonist, short half-life (30–90 min), first-line for opioid overdose; always consider infusion for long-acting opioids to prevent re-sedation. [cite: KD Tripathi 9e Ch 34]
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