## Management of Acute Opioid Overdose **Key Point:** Naloxone is a competitive opioid antagonist and the gold standard for acute opioid toxicity with respiratory depression. It rapidly reverses all opioid effects including respiratory depression, sedation, and miosis. ### Clinical Presentation Recognition The patient exhibits the classic **opioid toxicity triad**: 1. Respiratory depression (RR 8/min, normal 12–20) 2. Pinpoint pupils (miosis) 3. Altered mental status (CNS depression) The arterial blood gas confirms **acute respiratory acidosis** with hypoxia (PaO₂ 55 mmHg, normal >80) and hypercapnia (PaCO₂ 65 mmHg, normal 35–45). ### Why Naloxone is the Answer **High-Yield:** Naloxone dosing and administration: - **Initial dose:** 0.4–0.8 mg IV (can repeat every 2–3 minutes up to 10 mg total) - **Onset:** 1–2 minutes IV (faster than IM or intranasal) - **Duration:** 30–90 minutes (shorter than most opioids → risk of re-sedation) - **Mechanism:** Competitive antagonism at μ, δ, and κ opioid receptors **Clinical Pearl:** After naloxone administration, the patient must be monitored continuously for at least 2–4 hours because: - Naloxone's half-life (60–90 min) is shorter than morphine's (2–4 hours) - Re-sedation and recurrent respiratory depression are common - Mechanical ventilation support should be prepared in parallel ### Concurrent Management - Supplemental oxygen (non-rebreather mask initially, then titrate to SpO₂ >90%) - Bag-mask ventilation if naloxone unavailable or ineffective - IV access, continuous cardiac and pulse oximetry monitoring - Consider ICU admission if large opioid dose or long-acting formulation **Warning:** Do NOT delay naloxone while waiting for investigations or other interventions. This is a **life-threatening emergency** requiring immediate reversal. [cite:Harrison 21e Ch 467]
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