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Aims To measure and evaluate clinical response to nasal naloxone in opioid overdoses in the pre‐hospital environment. Design Randomised, controlled, double‐dummy, blinded, non‐inferiority trial, and conducted at two centres. Setting Participants were included by ambulance staff in Oslo and Trondheim, Norway, and treated at the place where the overdose occurred. Participants Men and women age above 18 years with miosis, rate of respiration ≤8/min, and Glasgow Coma Score <12/15 were included. Informed consent was obtained through a deferred‐consent procedure. Intervention and comparator A commercially available 1.4 mg/0.1 mL intranasal naloxone was compared with 0.8 mg/2 mL naloxone administered intramuscularly. Measurements The primary end‐point was restoration of spontaneous respiration of ≥10 breaths/min within 10 minutes. Secondary outcomes included time to restoration of spontaneous respiration, recurrence of overdose within 12 hours and adverse events. Findings In total, 201 participants were analysed in the per‐protocol population. Heroin was suspected in 196 cases. With 82% of the participants being men, 105 (97.2%) in the intramuscular group and 74 (79.6%) in the intranasal group returned to adequate spontaneous respiration within 10 minutes after one dose. The estimated risk difference was 17.5% (95% CI, 8.9%–26.1%) in favour of the intramuscular group. The risk of receiving additional naloxone was 19.4% (95% CI, 9.0%–29.7%) higher in the intranasal group. Adverse reactions were evenly distributed, except for drug withdrawal reactions, where the estimated risk difference was 6.8% (95% CI, 0.2%–13%) in favour of the intranasal group in a post hoc analysis. Conclusion Intranasal naloxone (1.4 mg/0.1 mL) was less efficient than 0.8 mg intramuscular naloxone for return to spontaneous breathing within 10 minutes in overdose patients in the pre‐hospital environment when compared head‐to‐head. Intranasal naloxone at 1.4 mg/0.1 mL restored breathing in 80% of participants after one dose and had few mild adverse reactions.

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Compressions during the insufflation phase of ventilations may cause severe pulmonary injury during cardiopulmonary resuscitation (CPR). Transthoracic impedance (TTI) could be used to evaluate how chest compressions are aligned with ventilations if the insufflation phase could be identified in the TTI waveform without chest compression artifacts. Therefore, the aim of this study was to determine whether and how the insufflation phase could be precisely identified during TTI. We synchronously measured TTI and airway pressure (Paw) in 21 consenting anaesthetised patients, TTI through the defibrillator pads and Paw by connecting the monitor-defibrillator’s pressure-line to the endotracheal tube filter. Volume control mode with seventeen different settings were used (5–10 ventilations/setting): Six volumes (150–800 mL) with 12 min−1 frequency, four frequencies (10, 12, 22 and 30 min−1) with 400 mL volume, and seven inspiratory times (0.5–3.5 s ) with 400 mL/10 min−1 volume/frequency. Median time differences (quartile range) between timing of expiration onset in the Paw-line (PawEO) and the TTI peak and TTI maximum downslope were measured. TTI peak and PawEO time difference was 579 (432–723) m s for 12 min−1, independent of volume, with a negative relation to frequency, and it increased linearly with inspiratory time (slope 0.47, R 2 = 0.72). PawEO and TTI maximum downslope time difference was between −69 and 84 m s for any ventilation setting (time aligned). It was independent ( R 2 < 0.01) of volume, frequency and inspiratory time, with global median values of −47 (−153–65) m s , −40 (−168–68) m s and 20 (−93–128) m s , for varying volume, frequency and inspiratory time, respectively. The TTI peak is not aligned with the start of exhalation, but the TTI maximum downslope is. This knowledge could help with identifying the ideal ventilation pattern during CPR.

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