 Prompt and early defibrillation of VF or pVT has become the standard of care. Drug therapy for shock resistant VF or pVT has been relegated to a secondary role since there is little evidence that these agents are of benefit. As a result, their use is considered indeterminate or class IIB. In addition, cardiac arrest and cardiopulmonary resuscitation are extreme forms of stress that lead to the highest catecholamine levels ever recorded in both human or experimental animal models. Endogenous catecholamine concentrations are high during ventricular fibrillation even in the absence of epinephrine administration. Currently, epinephrine is the vasopressor of choice for the treatment of cardiac arrest although vasopressin has been used as an alternative. Of note, vasopressin has been shown to be superior to epinephrine in patients with asystole however, its effects were similar to those of epinephrine in the management of VF or pulseless electrical activity. Furthermore, previous studies have raised concern that epinephrines beta adrenergic effect may increase the myocardial oxygen consumption of the fibrillating heart and predispose to post-defibrillation dysfunction and cardiac arrhythmias. 