Hyperkalemia and Ionized Hypocalcemia During Cardiac Arrest and Resuscitation: Possible Culprits for Postcountershock Arrhythmias?

Study objective: Early countershock of ventricular fibrillation (VF) has been shown to improve immediate and long-term outcome of out-of-hospital cardiac arrest. However, studies indicate that countershock of prolonged VF most commonly results in asystole or a nonperfusing bradyarrhythmia (pulseless electrical activity [PEA]), which rarely respond to current therapy. The cause of these postcountershock rhythm disturbances is not well understood but may be related to electrical injury of the globally ischemic myocardium or to local metabolic abnormalities that impair impulse formation and cardiac contraction. The purpose of this study was to evaluate changes in serum potassium and free calcium homeostasis during cardiac arrest and advanced cardiac life support (ACLS) interventions. Methods: After sedation, intubation, anesthesia, and instrumentation, VF was induced in 13 dogs. After 7.5 minutes of VF, animals were immediately countershocked, standard closed-chest CPR was initiated, and epinephrine was administered (1 mg in repeated doses if necessary). Results: Ten animals could not be resuscitated despite 20 minutes of ACLS interventions. In these animals, a progressive increase in serum potassium was observed from the onset of ACLS to the termination of resuscitation efforts (4.3±.6 to 6.0±.8 mEq/L, P