Abstract
The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents produce systemic vasoconstriction. This increases aortic diastolic pressure, and consequently, coronary and cerebral perfusion pressures. The pharmacologic responses to the adrenergic agents are mediated by a group of receptors that are classified as alpha (α), including α1, and α2, and beta (β), including β1 and β2. Epinephrine, which has each of these adrenergic actions, has been the preferred adrenergic agent for the management of cardiac arrest for almost 40 years. Its primary efficacy is due to its ca-adrenergic vasopressor effects. This contrasts with its β-adrenergic actions, which are inotropic, chronotropic, and vasodilator. Accordingly,,B-adrenergic actions prompt increases in myocardial oxygen consumption, ectopic ventricular arrhythmias, and transient hypoxemia due to pulmonary arteriovenous shunting. This may account for the failure to demonstrate that epinephrine improves ultimate outcomes in human victims of cardiac arrest. Major interest has more recently been focused on selective α-adrenergic agonists. Both α1,-agonists and α2-agonists are peripheral vasopressors. However, rapid desensitization of α-adrenergic receptors occurs during cardiopulmonary resuscitation. Moreover, ax-adrenergic receptors are present in the myocardium, and α1-agonists, like β-adrenergic agonists, increase myocardial oxygen consumption. If they cross the blood-brain barrier, α2-adrenoceptor agonists also have centrally acting vasodilator effects. In the absence of central nervous system access, α2-adrenergic agonists have selective peripheral vasoconstrictor effects. Under experimental conditions of cardiopulmonary resuscitation, selective α2-agonists, which do not gain entrance into the brain, produce only systemic vasoconstriction. Experimentally, these selective Ut2-agonists are as effective as epinephrine for initial cardiac resuscitation and have the additional advantage of minimizing myocardial oxygen consumption during the global myocardial ischemia of cardiac arrest. Accordingly, myocardial ischemic injury during cardiopulmonary resuscitation is minimized, and postresuscitation myocardial function is preserved with improved survival.