Introduction

  • The effects of epinephrine on animal hemodynamics have been studied since the late 1800s with
  • recent concern with deleterious complications with cerebral and myocardial oxygen supply.

  • Recently, there has been consideration for norepinephrine post cardiac arrest to minimize the
  • complications associated with epinephrine

    Epinephrine

    Norepinephrine

    Dose

    Weight-based dosing:

    ● Usual dosage range: 0.01 to 1

    mcg/kg/minute; titrate based on

    clinical end points (eg, MAP, end-

    organ perfusion)

    Non-weight-based dosing:

    ● Usual dosage range: 1 to 80

    mcg/minute; titrate based on

    clinical end points (eg, MAP, end-

    organ perfusion

    Institutional infusion rates may vary

    Weight-based dosing:

    ● Initial: 0.05 to 0.15 mcg/kg/minute; titrate

    based on clinical end points (eg, MAP, end-

    organ perfusion); usual dosing range: 0.05 to

    1 mcg/kg/minute

    Non-weight-based dosing (based on ~80 kg

    patient):

    ● Initial: 5 to 15 mcg/minute; titrate based on

    clinical end points (eg, MAP, end-organ

    perfusion); usual dosing range: 5 to 80

Clinical Detail

Drug Comparison

EpinephrineNorepinephrine
DoseWeight-based dosing:
• Usual dosage range: 0.01 to 1 mcg/kg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion)

Non-weight-based dosing:
• Usual dosage range: 1 to 80 mcg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion)

Institutional infusion rates may vary
Weight-based dosing:
• Initial: 0.05 to 0.15 mcg/kg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion); usual dosing range: 0.05 to 1 mcg/kg/minute

Non-weight-based dosing (based on ~80 kg patient):
• Initial: 5 to 15 mcg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion); usual dosing range: 5 to 80 mcg/minute

Institutional infusion rates may vary
PharmacokineticsOnset: Immediate
Distribution: 1-2 minutes to reach peak
Metabolism: rapid hepatic degradation
Elimination: urine (inactive metabolites)
Half-life: <5 minutes
Onset: Immediate
Distribution: 1-2 minutes to reach peak
Metabolism: rapid hepatic degradation
Elimination: urine (inactive metabolites)
Half-life: <5 minutes
Adverse EffectsTachyarrhythmias, myocardial ischemia, may decrease cerebral perfusion, mesenteric ischemia, extravasation leading to necrosis, lactic acidosisTachyarrhythmias, myocardial ischemia, extravasation leading to necrosis

Mechanism of Action

Receptor ActivityPharmacological ActionEffect
α agonistPeripheral vasoconstriction↑ myocardial and cerebral blood flow
β agonist↑ heart rate and contractility↑ myocardial oxygen demand

Evidence

Author (Year)Study Design/Patient PopulationInterventionResults
Bougouin, 2022Retrospective
N=766
• Norepinephrine infusion
• Epinephrine infusion
• All-cause hospital mortality was significantly higher in the epinephrine group (OR 2.6; 95%CI 1.4-4.7; P = 0.002).

• Proportion of patients with CPC of 3-5 at hospital discharge was also higher with epinephrine
Weiss, 2021Retrospective
N=93
• Norepinephrine infusion
• Epinephrine infusion
• Significantly more EPI patients had refractory hypotension, rearrest, or death in the emergency department (EPI 21/42, 50% vs. NE 10/45, 22.2%; P = 0.008)

• In an adjusted regression model, the odds of reaching the primary outcome in the ED were 3.94 [95%CI 1.38-12.2] (P = 0.013) times higher in the EPI group compared to NE treated patients.
Mion, 2014Case report
N=1
• Epinephrine then transition to norepinephrine• 58 year male, The cardiac rhythm turned into a ventricular fibrillation (VF). That had reccurent v fib with epinephrine

• Return of spontaneous circulation was observed, with the recovering of sinusal activity. After staying for several weeks in intensive care unit because of multiorgan failure, the patient recovered without sequelae.
Kim, 2012Retrospective
N=90
• Norepinephrine infusion
• Epinephrine infusion
• The survivors (N=46) were more likely to have received norepinephrine infusion than the non-survivors (34.8% vs 22.6%).

• Of those who had a prolonged arrest (more than ten minute down time, N=28) the survivors were also more likely to have received norepinephrine infusion (42.85% vs 25%).

Conclusions

● It’s controversial as to whether epinephrine is preferred vasopressor post cardiac arrest.

● Norepinephrine is a reasonable agent to use post arrest if it is clinically warranted.

References

7/30/2025

● Micromedex [Electronic version].Greenwood Village, CO: Truven Health Analytics. Accessed 2022,

March 15.

● http://www.micromedexsolutions.com/

● Callaway C. Epinephrine for cardiac arrest. Current Opinion in Cardiology. 2013;28(1):36-42.

● Epinephrine [package insert] Lake Forest, IL: Hospira, Inc.; 2019.

● (poster) Kim et al. THE BENEFIT OF NOREPINEPHRINE INFUSION FOR HEMODYNAMIC

SUPPORT FOLLOWING CARDIOPULMONARY ARREST AND RESUSCITATION. Critical Care

Medicine: December 2012 – Volume 40 – Issue 12 – p 1-328

● Mion Get al. Cardiac arrest: should we consider norepinephrine instead of epinephrine? Am J

Emerg Med. 2014 Dec;32(12):1560.e1-2. PMID: 24997106.

● Weiss A, et ql. Comparison of Clinical Outcomes with Initial Norepinephrine or Epinephrine for

Hemodynamic Support After Return of Spontaneous Circulation. Shock. 2021 Dec 1;56(6):988-993.

PMID: 34172611.

● Bougouin W, et al. Epinephrine versus norepinephrine in cardiac arrest patients with post-

resuscitation shock. Intensive Care Med. 2022 Mar;48(3):300-310. PMID: 35129643.

Tags:norepinephrine epinephrine post cardiac arrest shock