Arrhythmia and acute coronary syndrome suppression and cardiac resuscitation management with bretylium.
It is well known that electric shock can both initiate and terminate ventricular fibrillation. Refractory ventricular fibrillation (RVF) may often be an iatrogenic paradoxical result of early, frequent, excessive salvos of DC current countershocks and inappropriate off-label drug use, particularly aggressive epinephrine administration. Evidence suggests that the current advanced cardiac life support pharmacology protocol for cardiac resuscitation may contribute to disappointing survival in patients with out-of-hospital cardiac arrest. Controlled studies and new theoretical consideration suggest the protocol may induce RVF. In contrast, studies suggest that immediate adequate intravenous bretylium administration therapy together with sustained effective chest compressions can induce chemical defibrillation or facilitate electrical defibrillation as well as reduce the intensity, or even need for potentially heart-damaging countershock, where early frequent excessive current shocks are likely to increase refractory arrhythmia as demonstrated in animals and in humans. Salvos of shocks do not allow time between shocks for uniform recovery of normal electrical parameters needed to restore a stable heart rhythm. This may occur by inadvertently administering shock during the vulnerable period of the cardiac cycle. There are compelling existing data to demonstrate that bretylium and cardiopulmonary resuscitation (CPR) delivered before initiating shock therapy is likely to provide the best outcome in cardiac arrest. But, most importantly, adequate CPR chest compressions administered while bretylium is being infused also provide the opportunity to wash out electrically destabilizing electrolytes that have leaked from or are abnormally transported by functionally damaged membranes of fibrillation-induced ischemic myocytes. This may cause abnormal compartment redistribution of electrolytes that may facilitate RVF by heterogeneously partially depolarizing ischemic myocytes. Although efforts have been made to provide hard science for advanced life support, the guidelines are a product of consensus, the give and take of collegiality and intuition rather than rigorous controlled studies. Bretylium has a direct antifibrillatory action normalizing myocyte membrane currents, which restores intracompartmental normal electrolyte balance. In addition, adrenergic blockade by bretylium dilates coronary arteries, increasing effective O2 delivery by CPR. The free and aggressive use of epinephrine is toxic. Catechalomines cause coronary spasm and puts myocardial metabolism into damaging hypermetabolic overdrive to support the "fight or flight reflex" rapidly depleting adenosine triphosphate needed for cardiac electrical and mechanical recovery. Moreover, the value of epinephrine to resuscitation has never been demonstrated in a controlled human study, whereas its potential damage has been largely ignored. Epinephrine's potential deleterious actions that might compromise resuscitation are well established and reviewed here.
Bacaner
Marvin
M
Department of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN 55416, USA. hbacaner@comcast.net
Dembo
Donald H
DH
D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000628:therapy; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy* / Q000628:therapy; D001949:Bretylium Compounds / Q000008:administration & dosage / Q000627:therapeutic use*; D016887:Cardiopulmonary Resuscitation; D004837:Epinephrine / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans
D000889:Anti-Arrhythmia Agents; D001949:Bretylium Compounds; C045166:bretylium; D004837:Epinephrine