Calcium and its role in cardiac arrest: understanding the controversy.
Calcium ions play a critical role in excitation-contraction coupling in the myocardial cell, leading to enhanced automaticity and contractility. For these reasons the American Heart Association and the National Academy of Science-National Research Council has advocated its use in cardiac arrest due to asystole and electromechanical dissociation (EMD). However, increasing evidence suggests that calcium has been of little benefit in cardiac arrest not only because of the poor salvage rates (0%-8%) of victims in asystole or EMD and the dangerously high serum calcium levels following standard calcium administration, but also because of the cellular accumulation of calcium within the myocardium that occurs during cardiac arrest. In fact, some authors advocate the use of calcium channel blockers in protecting myocardial tissue during anoxia. Therefore the usefulness of calcium in asystole and EMD is highly suspect and must be reevaluated.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology; D004734:Energy Metabolism; D006323:Heart Arrest / Q000188:drug therapy / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D006706:Homeostasis; D006801:Humans; D006996:Hypocalcemia / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D012151:Resuscitation / Q000379:methods; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000188:drug therapy
D002121:Calcium Channel Blockers; D000255:Adenosine Triphosphate; D002118:Calcium