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Background <p>Prolonged resuscitation is associated with poor patient outcomes. While the importance of bystander CPR and early defibrillation is well-known, the role of other components affecting resuscitation duration is less well-established. We postulated that first-dose intraosseous (IO) epinephrine would prolong the pressor-to-ROSC interval compared to intravenous (IV) drug administration.</p> Aims <p>To describe the relationship between first epinephrine administration route and pressor-to-ROSC intervals.</p> Methods <p>A retrospective analysis of the 2020 ESO Data Collaborative Annual Research dataset was conducted among adults who experienced non-traumatic, bystander-witnessed arrests. A Cox proportional hazard model was used to determine the influence of first epinephrine route on the pressor-to-ROSC interval. End-of-event was defined as ROSC, field termination of resuscitation, or hospital arrival without ROSC, with right censoring of the latter group.</p> Results <p>Overall, 9351 patients were included for analysis, of which 63.9% were males. The mean age of participants was 65.3(± 15.5) years and presumed cardiac etiology was present in 82.7% of arrests. An initial shockable rhythm was present in 27.1%, while 29.7% received bystander CPR and 39.7% attained ROSC. The mean pressor-to-ROSC interval was 13.21(± 9.65), 14.86 (± 10.89), and 14.42 (± 10.52) minutes for the intravenous, tibial IO, and humeral IO routes, respectively (<i>p</i> &lt; 0.001). First epinephrine administration via the tibial or humeral IO route was associated with a decreased hazard of ROSC compared to the IV route (HR = 0.78, <i>p</i> &lt; 0.001 and HR = 0.86, <i>p</i> = 0.01 per minute, respectively).</p> Conclusions <p>These data suggest that the tibial and humeral IO routes of first epinephrine administration were associated with marginally prolonged resuscitation duration after drug administration and decreasing hazard of ROSC.</p>

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Intraosseous route is associated with prolonged epinephrine-to-ROSC interval in out-of-hospital cardiac arrest

  • 期刊论文

  • 发表日期：

    2025年6月21日

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  • Michael W. Hubble,
  • Stephen Taylor,
  • Melisa Martin,
  • Sara Houston,
  • Ginny R. Kaplan,
  • Randy D. Kearns

摘要

Background

Prolonged resuscitation is associated with poor patient outcomes. While the importance of bystander CPR and early defibrillation is well-known, the role of other components affecting resuscitation duration is less well-established. We postulated that first-dose intraosseous (IO) epinephrine would prolong the pressor-to-ROSC interval compared to intravenous (IV) drug administration.

Aims

To describe the relationship between first epinephrine administration route and pressor-to-ROSC intervals.

Methods

A retrospective analysis of the 2020 ESO Data Collaborative Annual Research dataset was conducted among adults who experienced non-traumatic, bystander-witnessed arrests. A Cox proportional hazard model was used to determine the influence of first epinephrine route on the pressor-to-ROSC interval. End-of-event was defined as ROSC, field termination of resuscitation, or hospital arrival without ROSC, with right censoring of the latter group.

Results

Overall, 9351 patients were included for analysis, of which 63.9% were males. The mean age of participants was 65.3(± 15.5) years and presumed cardiac etiology was present in 82.7% of arrests. An initial shockable rhythm was present in 27.1%, while 29.7% received bystander CPR and 39.7% attained ROSC. The mean pressor-to-ROSC interval was 13.21(± 9.65), 14.86 (± 10.89), and 14.42 (± 10.52) minutes for the intravenous, tibial IO, and humeral IO routes, respectively (p < 0.001). First epinephrine administration via the tibial or humeral IO route was associated with a decreased hazard of ROSC compared to the IV route (HR = 0.78, p < 0.001 and HR = 0.86, p = 0.01 per minute, respectively).

Conclusions

These data suggest that the tibial and humeral IO routes of first epinephrine administration were associated with marginally prolonged resuscitation duration after drug administration and decreasing hazard of ROSC.