Abstract 201: Beta-Adrenergic Stimulation Promotes Early Electrical Failure During Simulated VF-Induced Cardiac Arrest And Delays Electrical Recovery Upon Reperfusion
During cardiac arrest adrenergic stimulation is enhanced due to both endogenous increase in myocardial tissue catecholamine levels and exogenous epinephrine administration during resuscitation. Whereas alpha-adrenergic stimulation may be beneficial for hemodynamic recovery, there is growing evidence that beta-adrenergic stimulation is detrimental. Clinically, there is controversy as to whether epinephrine administration improves overall survival in cardiac arrest. Here we investigated the effects of beta-adrenergic stimulation on electrical activity during simulated ventricular fibrillation (VF) [[Unable to Display Character: –]] induced cardiac arrest and subsequent reperfusion. We performed optical mapping of the voltage-sensitive dye RH237 in the anterior right and left ventricles (RV and LV) of Langendorff-perfused rabbit hearts subjected to normothermic global no-flow ischemia and rapid pacing (cycle length 200 ms) in the presence or in the absence of isoproterenol (ISO, 30 nM). 2,3-butanedione monoxime (20 mM) was used to reduce motion artifact. Excitable area was measured in optical maps based on the criterion of the minimum time-derivative of the upstroke of the optical action potential. ISO markedly accelerated electrical depression in both LV and RV (more in LV) compared to control hearts (see Figure, * indicate comparisons with significant difference between groups at p<0.05). In addition, ISO delayed recovery of electrical activity upon reperfusion (62±14% recovery in ISO vs.98±2% recovery in control at 5 min of reperfusion, p<0.01). Furthermore, ISO tended to increase the incidence of post-reperfusion arrhythmias compared to control (83% vs. 25%, respectively; p=NS). We conclude that beta-adrenergic stimulation aggravates electrical dysfunction under conditions typically present during cardiac arrest/resuscitation, which might contribute to the overall detrimental outcomes of natural or induced catecholamine increase in this setting.
- © 2013 by American Heart Association, Inc.