The roles of methoxamine and norepinephrine in electromechanical dissociation

Electromechanical dissociation (EMD) in patients in cardiac arrest is associated with a poor prognosis. Pressor agents, particularly alpha-agonists, have proven to be useful in resuscitation from asphyxial and fibrillatory arrest in the animal model. Beta-agonists, such as isoproterenol, have not been shown to improve the resuscitation rate. The standard pressor used in all forms of cardiac arrest is epinephrine. The key question that must be considered is whether methoxamine or norepinephrine is superior to epinephrine in resuscitating patients in cardiac arrest. Methoxamine is a pure alpha 1 agonist causing vasoconstriction and increased peripheral vascular resistance. Norepinephrine and epinephrine demonstrate activity at alpha 1, alpha 2, beta 1, and beta 2 receptor sites. Does alpha 2 and beta activity help or hinder resuscitation? Beta activity on the myocardium will increase oxygen consumption (inotropic and chronotropic effects), may predispose to arrhythmias, and will shunt blood from the endocardium to the epicardium. On the other hand, there is evidence that beta agonists increase coronary and cerebral blood flow. Outcome studies have shown methoxamine to be comparable to epinephrine in resuscitation from asphyxial arrest. One study demonstrated methoxamine's superiority in raising the aortic diastolic pressure and resuscitating animals from ventricular fibrillation. No significant advantage of norepinephrine use is evident in the literature. Controlled experiments in the animal model and in human patients must be done to determine whether methoxamine or epinephrine is superior in resuscitation from EMD and other forms of cardiac arrest.