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  • Title: Is a pressor necessary during aortic perfusion and oxygenation therapy of cardiac arrest?
    Author: Paradis NA.
    Journal: Ann Emerg Med; 1999 Dec; 34(6):697-702. PubMed ID: 10577397.
    Abstract:
    STUDY OBJECTIVE: Occlusion of the descending aorta and infusion of oxygenated ultrapurified polymerized bovine hemoglobin may improve the efficacy of advanced cardiac life support (ACLS). Because selective aortic perfusion and oxygenation (SAPO) directly increases coronary perfusion pressure, exogenous epinephrine may not be required. The purpose of this study was to determine whether exogenous epinephrine is necessary during SAPO by comparing the rate of return of spontaneous circulation and aortic and coronary perfusion pressures during ACLS-SAPO in animals treated with either intra-aortic epinephrine or saline solution. METHODS: A prospective, randomized, interventional before-after trial with a canine model of ventricular fibrillation cardiac arrest and ACLS based on external chest compression was performed. The ECG, right atrial, aortic arch, and esophageal pulse pressures were measured continuously. A descending aortic occlusion balloon catheter was placed through the femoral artery. Ventricular fibrillation was induced, and no therapy was given during the 10-minute arrest time. Basic life support was then initiated and normalized by standardization of esophageal pulse pressure and central aortic blood gases. After 3 minutes of basic life support, the aortic occlusion balloon was inflated, and 0.01 mg/kg epinephrine or saline solution was administered through the aortic catheter followed by 450 mL of ultrapurified polymerized bovine hemoglobin over 2 minutes. Defibrillation was then attempted. The outcomes and changes in intravascular pressures were compared. RESULTS: Aortic pressures were higher during infusions in animals treated with epinephrine. During infusion, the mean aortic relaxation pressure increased by 58+/-5 mm Hg in animals that had received epinephrine versus 20+/-11 mm Hg in those that had received saline placebo. The coronary perfusion pressure during infusion increased by 52+/-8 mm Hg in animals that had received epinephrine versus 26+/-10 mm Hg in those that had received saline. Only 2 of 7 animals in the placebo group had return of spontaneous circulation versus 7 of 8 in the epinephrine group. CONCLUSION: The addition of epinephrine to ACLS-SAPO increases vital organ perfusion pressures and improves outcome from cardiac arrest. There appears to be a profound loss of arterial vasomotor tone after prolonged arrest. This loss of vasomotor tone may make exogenous pressors necessary for resuscitation after prolonged cardiac arrest.
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