PHARMACOLOGICAL CONTROVERSIES IN CPR

Since the 1985 Emergency Cardiac Care Conference, numerous controversies about the pharmacology of CPR have arisen (eg, questions about the pharmacokinetics and pharmacodynamics of drugs during CPR, the optimal vehicle for delivery of medications, and the dose of atropine in brady-asystolic cardiac arrest). This article has three objectives: 1) to critically explore these controversies, 2) to provide recommendations for clinical practice, and 3) to identify areas for future study. The ideal route is one which combines rapid access with quick delivery of drug to the central circulation. Because of hemodynamic changes during CPR, administration of drugs into the central circulation is preferable when compared with peripheral venous injection. Whenever drugs are administered from a peripheral IV site, the extremity should be elevated, and a 20-mL bolus of IV fluid should be given to facilitate access of the agent to the central circulation. If there is a delay in obtaining venous access, epinephrine, lidocaine, and atropine may be administered through the endotracheal tube at 2.5 times the IV dose. When administering these drugs through the endotracheal tube, dilute the drug in 10 mL of saline or water and inject it through a long catheter beyond the tip of the endotracheal tube. Dextrose 5% water is the primary vehicle for drug delivery during CPR. However, the administration of glucose during CPR is controversial because of the potentially detrimental effects of hyperglycemia on neuronal function during periods of ischemia. Data are inconclusive regarding the effects of glucose levels on neurologic outcome following resuscitation. Hyperglycemia may be a marker for prolonged resuscitation with subsequent impairment in insulin release. However, inappropriately low levels of insulin during CPR may adversely affect myocardial glucose utilization. Further studies are needed to examine the potential role of insulin therapy in cardiac arrest victims with hyperglycemia. Supplemental administration of glucose should be reserved for documented hypoglycemia. The following issues regarding the use of atropine in cardiac arrest remain unresolved and warrant discussion: what is the maximum vagolytic dose of atropine in human beings, and will a higher dose of atropine change the outcome of patients with brady-asystole? Several studies have explored the dose response to atropine in human beings; 0.04 mg/kg (3 mg for a 70-kg patient) appears to be the maximum vagolytic dose of atropine. Although there are good theoretical reasons to use atropine in brady-asystolic cardiac arrest, human studies suggest that atropine may have only a limited role. It remains to be determined if increasing the maximum dose of atropine to 0.04 mg/kg will change the clinical outcome of patients with brady-asystole.