Original Contribution Vasopressin alone or with epinephrine may be superior to epinephrine in a clinically relevant porcine model of pulseless electrical activity cardiac arrest Charles M. Little DO a, * , Mia H. Marietta MS b , Kathleen Peng c , Kennon Heard MD a , Miguel Fragoso DVM d , Fred A. Severyn MD a , Vikhyat S. Bebarta MD a , Norman A. Paradis MD a a Division of Emergency Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA b School of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA c University of Colorado at Boulder, Denver, CO, USA d Department of Cardiovascular Physiology, University of Colorado Health Sciences Center, Denver, CO 80262, USA Received 21 January 2006; revised 31 March 2006; accepted 7 May 2006 1. Introduction Cardiac arrest remains an important entity in the clinical field. In the United States, annually there are about 450,000 sudden cardiac deaths in the prehospital or ED setting [1]. Current survival rates are about 5% to 10% of cardiac arrest cases, as reported in a recent European multicenter trial [2]. The presenting rhythm of cardiac arrest has changed over the last decade. The incidence of primary ventricular fibrillation (VF) is decreasing and the incidence of pulseless electrical activity (PEA) is increasing [3]. The widespread introduction of automated external defibrillators in the lay setting can be expected to increase the incidence of postcounter shock PEA. Pulseless electrical activity has a worse prognosis than VF [2]. Epinephrine the is currently recommended medical therapy for PEA [4]. Epinephrine increases coronary perfusion pressure (CoPP) and myocardial perfusion. Epinephrine-induced b 1 effects might be expected to increase myocardial contractility and rate in PEA, thus increasing cardiac output. However, use of epinephrine could increase the myocardial oxygen demand, resulting in supply-demand mismatch in ischemic myocardium [5]. Vasopressin has more recently been introduced in the treatment of cardiac arrest. Although a known coronary artery vasoconstrictor, vasopressin has been shown to increase myocardial blood flow in the setting of cardiac arrest [6,7]. A recent large European prehospital cardiac arrest study comparing epinephrine to vasopressin showed similar resuscitation rates with both drugs in PEA [2]. Of note, in this clinical study subjects who failed to respond to vasopressin had crossover to epinephrine, but the epinephrine group did not cross over to vasopressin. Drug treatment in animals in PEA has yielded mixed results. The use of different models of PEA has further confused the issue. Asphyxial bpediatricQ cardiac arrest models may differ significantly at the cellular level from the badultQ model of PEA after VF and defibrillation [8]. Direct comparison of vasopressin and epinephrine demon- strated improved outcome with epinephrine in an asphyxial swine model [9]. The same investigators found that 0735-6757/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2006.05.002 Presented in part at the Society for Academic Emergency Medicine Annual Meeting, May 2003, Orlando, Fla. * Corresponding author. Tel.: +1 303 372 5582. E-mail address: charles.little@uchsc.edu (C.M. Little). American Journal of Emergency Medicine (2006) 24, 810–814 www.elsevier.com/locate/ajem