• James T Niemann, John Rosborough, Scott Youngquist, Roger J Lewis, Quynh T Phan, and Scott Filler.
• Department of Emergency Medicine, Harbor-UCLA Medical Center, Torrance, CA, USA. jniemann@emedharbor.edu
• Acad Emerg Med. 2008 Oct 1; 15 (10): 939-44.

ObjectivesA systemic inflammatory response has been reported following resuscitation from cardiac arrest. The purpose of this study was to compare the magnitude of the tumor necrosis factor-alpha (TNF-alpha) response in two different swine models of ventricular fibrillation (VF) arrest.MethodsThis was a randomized comparative trial conducted with domestic swine (N = 28, mean weight 40 kg, range 34-49 kg) of both genders. Anesthetized and instrumented swine were randomized to electrically induced VF (n = 14) or spontaneous VF induced by occlusion of a coronary artery (n = 14). After 8 minutes of VF, countershocks were given and standard advanced cardiac life support was initiated. Resuscitated animals were observed for 3 hours, and hemodynamics, base excess, and TNF-alpha concentrations were measured at intervals.ResultsTNF-alpha concentrations were significantly greater in the ischemic VF group throughout the postresuscitation period. Multivariate modeling demonstrated that the TNF-alpha level was dependent on the method of VF induction and correlated with ischemia time (untreated VF period plus time to restoration of circulation) and the degree of postresuscitation hypoperfusion as reflected in base excess measurements.ConclusionsThis study demonstrates that TNF-alpha concentrations increase after resuscitation from cardiac arrest and that the TNF-alpha response is more profound in animals subjected to ischemic, spontaneous VF. The observed differences may be due to a longer resuscitation time and persistent postresuscitation hypoperfusion in the ischemic VF group. These differences need to be considered in studies evaluating mechanisms of postresuscitation organ dysfunction and defining mortality markers.

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