Epinephrine in Resuscitation: Curse or Cure?

Robert R Attaran; Gordon A Ewy

Disclosures

Future Cardiol. 2010;6(4):473-482. 

In This Article

Human Studies of Epinephrine in Cardiac Arrest

To date, no randomized controlled human trial has specifically evaluated early epinephrine administration in cardiac arrest and CPR. While several observational studies have reported on epinephrine usage for OHCA, their design features and limitations have resulted in findings that cannot be applied to modern approaches to OHCA.[71–73]

The most recent randomized controlled trial of the use of epinephrine together with other drugs in OHCA was conducted by Olasveengen et al. in Norway.[74] Adults with confirmed nontraumatic cardiac arrest were randomized to ACLS with – versus without – intravenous drug administration during the resuscitation effort. The 'no intravenous' group did not have an intravenous access established until an average of 5 min after ROSC. After exclusions, 433 patients were randomized to the intravenous arm versus 418 in the no intravenous arm. In approximately 62% of cases, the arrests were witnessed and bystander basic life support was reported to be initiated in almost all patients with witnessed arrest. Approximately a third of the patients had an initial rhythm that was shockable (VF or pulseless ventricular tachycardia). There were equivalent hands-off ratios and compression and ventilation rates between the two groups. However, there were some dissimilarities. The intravenous group demonstrated longer CPR duration (p < 0.001) and more shocks delivered (p = 0.008). There was a tendency towards less asystole but more pulseless electrical activity in the intraveous group (p = 0.06).

There was better short-term survival in the intravenous group.[74] A total of 40% achieved ROSC versus only 25% in the no intravenous group (p < 0.001). More intravenous group patients survived to hospital admission (43 vs 29%, p < 0.001). In the subgroup with asystole or pulseless electrical activity, the ROSC rate was improved by threefold better in the intravenous group (p < 0.001), although this advantage did not carry over to hospital discharge. In the subgroup with shockable rhythms (VF or pulseless ventricular tachycardia), no differences in ROSC, hospital admission or discharge rates were found between the intravenous versus no intravenous groups. The study found no difference in survival to hospital discharge or survival with good neurological outcome between the two approaches. Furthermore, there was no postarrest difference in survival at 1 month or 1 year. The authors note that this study may have been too underpowered to prove a difference. In summary, this prospective, single-center study demonstrated that early intravenous administration of epinephrine, atropine and/or amiodarone during OHCA was associated with improved ROSC, but not longer-term survival. Notably, the authors did not find epinephrine usage to be an independent predictor of poor outcome.[74]

This study found that the late administration of epinephrine during OHCA did not result in improved hospital discharge.[74] The mean ambulance response time was 10 min. The time between ambulance arrival and intravenous administration was not provided. What one can conclude from this report is that the late administration of epinephrine did not appear to be helpful. However, since individuals with nonshockable rhythms (the group known to have worse outcomes) had a higher ROSC, and the fact that patients with OHCA and ROSC are significantly more likely to survive to hospital discharge, one could argue that this study supported the use of epinephrine in OHCA. The most powerful predictor by far of survival to hospital discharge is ROSC in the field.[75] This finding is evidence that the battle to save victims of OHCA is won or lost at the scene.

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