Epinephrine in Resuscitation: Curse or Cure?

Robert R Attaran; Gordon A Ewy


Future Cardiol. 2010;6(4):473-482. 

In This Article

Pharmacologic & Physiologic Considerations: The Importance of Coronary Perfusion Pressure

It is now known that there are subtypes of both the α- and β-adrenergic receptors and that epinephrine's effects are mediated through α1-, α2-, β1- and β2-receptors.[16–23] Its nonselective agonist profile results in a host of effects.[24] The α1-receptors mediate arteriolar vasoconstriction and are also positively inotropic, chronotropic and may induce coronary vasoconstriction. The α2-receptors mediate venoconstriction, among other effects. The β1- and β2-receptors induce positive inotropy and chronotropy and can also vasodilate the coronaries.

To paraphrase what Crile and Dolley stated over a century ago: the secret of resuscitation seems to be to increase the aortic diastolic pressure. It turns out that they were correct.[11] During resuscitation efforts, coronary perfusion pressures (aortic diastolic minus right atrial diastolic pressure) above 15 mmHg during resuscitation are associated with improved return of spontaneous circulation (ROSC) in both humans and animals[25,26] and increased survival in animals.[26] During resuscitation from cardiac arrest, epinephrine improves coronary and cerebral perfusion.[27–30]

Wegria et al. induced VF in experiments and observed that epinephrine could alter the ECG VF character from coarse and slow (the variant observed in late-stage VF) to fine and rapid.[31]

However, epinephrine also has adverse effects. It increases myocardial oxygen consumption,[32] postresuscitation myocardial dysfunction[33] and ventricular arrhythmias.[34] Ristagno et al. suggest that microcirculation to the superficial areas of the brain is decreased with epinephrine.[35] Lindberg et al. propose that epinephrine may reduce overall cardiac output since blood flow to nonvital organs falls to almost zero owing to vasoconstriction.[36] This may induce ischemia in underperfused organs (e.g., bowel) and lead to an inflammatory response following successful resuscitation.[37,38] There is also some evidence that epinephrine may induce hypokalemia,[39] platelet aggregation[40] and oxidative damage.[41,42]

During resuscitation efforts, end-tidal CO2 has been shown to reflect pulmonary blood flow,[43,44] coronary perfusion pressure[36] and improved outcomes in OHCA.[45] Lindberg et al., using a swine model, administered epinephrine or norepinephrine during CPR and defibrillated 4 min later.[36] These vasopressors improved coronary perfusion pressure but reduced end-tidal CO2 and pulmonary flow. Thrush et al. demonstrated increased intrapulmonary shunting and hypoxia with epinephrine during CPR.[46] They proposed β-mediated pulmonary vasoconstriction as a possible factor. In a rat asphyxial cardiac arrest model, epinephrine use was associated with increased mortality.[47]


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