![]() High-quality CPR should be administered while giving epinephrine, and after the initial dose, epinephrine is given every 3-5 minutes.įor PEA a rhythm and pulse check should be performed after 5 cycles of CPR. When treating PEA, epinephrine can be given as soon as possible but its administration should not delay the initiation or continuation of CPR. Vasoconstriction is important during CPR because it will help increase blood flow to the brain and heart. The vasopressor that is used for the treatment within the right branch of the Cardiac Arrest Algorithm is epinephrine.Įpinephrine is primarily used for its vasoconstrictive effects. ![]() ![]() Medications used in PEA VasopressorsĪ vasopressor is a medication that produces vasoconstriction and a rise in blood pressure. Identification and correction of the cause of PEA. Because survival from this type of cardiac arrest is so low, we are studying the mechanisms whereby pulseless electrical activity occurs, and we are also developing improved therapies for treating pulseless electrical activity, based on those mechanisms.Positive outcome of an attempted resuscitation depends primarily on two actions: 1. Many of these arrests are due to pulseless electrical activity, in which ther is relatively normal electrical activity of the heart, but no effective heart contractions. There are at least 500,000 victims of cardiac arrest each year in the United States. These studies should provide new information and insights about the pathophysiology of PEA cardiac arrests, and may lead to substantial improvements in the now dismal outcomes from PEA cardiac arrests. The goals of this project are to improve our understanding of the pathophysiology of PEA cardiac arrest, develop improved methods for augmenting blood flow during resuscitation, and also develop synergistic, improved strategies for mitigating the effects of the profound ischemia and/or hypoxia present in PEA arrest. Finally, we hypothesize that each of these strategies will have incremental and additive improvement in outcomes from PEA cardiac arrest. Additional preservation strategies may also be useful, including intra-arrest hypothermia. Controlled reperfusion, including post conditioning, may be necessary at the beginning of reperfusion to reduce reperfusion injury. Methods for augmenting blood flow should include the use of improved external compression devices, which may be particularly useful for treating out-of-hospital arrests and the use of extracorporeal systems, which may be particularly useful for in-hospital arrests. Therapy should, therefore, be directed at generating substantial blood flow during resuscitation, including the use of vasodilators, to reverse the profound ischemia that may be present. In addition, the already severe compromise of the metabolic status of the heart would make any degree of reperfusion injury more detrimental in PEA arrests than in VT/VF arrests. Even though there may be preconditioning, such preconditioning may not be uniform. We hypothesize, therefore, that therapy for PEA arrests must be directed at reversing this profound ischemia and/or hypoxia, as well as mitigating reperfusion injury. We further hypothesize that this chronic ischemia and/or hypoxia induces preconditioning, which prevents or delays the occurrence of VF, resulting in PEA arrest. This contrasts with most VT/VF arrests where acute ischemia causes VT/VF in a healthier substrate. We present the novel hypothesis that most PEA arrests are due to failure of ventricular muscle from acute ischemia and/or hypoxia in a substrate where there has been chronic ischemia and/or hypoxia. Defibrillation is the definitive treatment for VT/VF arrest, but is not indicated in PEA arrest. ![]() This critical need is most apparent with PEA arrests, since little is known about the pathophysiology or the optimal treatment of these arrests, especially when compared to VT/VF arrests. There is a critical need, therefore, for improved resuscitation strategies, since each 1% increase in survival rate would result in approximately 5000 additional survivors. The survival rates for PEA and asystolic arrests are much lower, however, and average only around 5%. The survival rates for VT/VF arrests average around 20%. In the majority of these patients, the initial rhythm is not ventricular fibrillation (VF) or ventricular tachycardia (VT), but is pulseless electrical activity (PEA) or asystole. ![]() ![]()
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