Evolving role of vasopressin in the treatment of cardiac arrest.

Sudden cardiac arrest is a major public heath problem, affecting more than 450,000 individuals annually. Response time and the initiation of cardiopulmonary resuscitation (CPR) remain the most important factors determining successful revival. During resuscitation, sympathomimetics are given to enhance cerebral and coronary perfusion pressures in an attempt to achieve restoration of spontaneous circulation. Epinephrine has been the preferred vasopressor since the inception of advanced cardiac life support, although the lack of definitive evidence regarding its effectiveness has created much controversy surrounding its use, including the optimum dosage. Vasopressin is an alternative vasopressor that, when given at high doses, causes vasoconstriction by directly stimulating smooth muscle V1 receptors. The 2000 American Heart Association (AHA) guidelines commented that vasopressin is a reasonable first-line vasopressor in patients with ventricular fibrillation or pulseless ventricular tachycardia. Since release of those guidelines, additional human studies support an expanded role for vasopressin, whereas other studies cast doubt regarding its efficacy compared with epinephrine. The AHA recently released revised guidelines for CPR and emergency cardiovascular care. The consensus was that vasopressors should remain a part of pulseless sudden cardiac arrest management, with epinephrine 1 mg every 3-5 minutes being the recommended adrenergic of choice. In these revised guidelines, the role of vasopressin expanded beyond previous recommendations, despite the recommendation being downgraded to class indeterminate. The guidelines comment that one dose of vasopressin 40 U may replace the first or second dose of epinephrine in all pulseless sudden cardiac arrest scenarios, including asystole and pulseless electrical activity. A consistent theme with all vasopressors in sudden cardiac arrest is that additional studies are necessary to clearly document greater efficacy compared with no treatment. Further evaluation is warranted to better assess the role of vasopressin in asystolic sudden cardiac arrest, as well as its use with epinephrine, and to determine its optimal timing of administration and potential synergistic effects.