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CARDIOVASCULAR ANESTHESIA

Vasopressor Response in a Porcine Model of Hypothermic Cardiac Arrest Is Improved with Active Compression-Decompression Cardiopulmonary Resuscitation Using the Inspiratory Impedance Threshold Valve

Claus Raedler, MD^*, Wolfgang G. Voelckel, MD^*, Volker Wenzel, MD^*, Ludger Bahlmann, MD, Wolfgang Baumeier, MD, Christian A. Schmittinger^*, Holger Herff^*, Anette C. Krismer, MD^*, Karl H. Lindner, MD^*, and Keith G. Lurie, MD

*Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University, Innsbruck, Austria; Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota; and the Department of Anesthesiology, Medical University, Lübeck, Germany

Address correspondence to Dr. Claus Raedler, Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to claus.raedler{at}uibk.ac.at Address reprint requests to Dr. Karl H. Lindner, Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University, Anichstrasse 35, 6020 Innsbruck, Austria.

During normothermic cardiac arrest, a combination of active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) with the inspiratory threshold valve (ITV) significantly improves vital organ blood flow, but this technique has not been studied during hypothermic cardiac arrest. Accordingly, we evaluated the hemodynamic effects of ACD + ITV CPR before, and after, the administration of vasopressin in a porcine model of hypothermic cardiac arrest. Pigs were surface-cooled until their body core temperature was 26°C. After 10 min of untreated ventricular fibrillation, 14 animals were randomly assigned to either ACD CPR with the ITV (n = 7) or to standard (STD) CPR (n = 7). After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after 28 min of cardiac arrest, including 18 min of CPR. Before the administration of vasopressin, mean ± SEM common carotid blood flow was significantly higher in the ACD + ITV group com-pared with STD CPR (67 ± 13 versus 26 ± 5 mL/min, respectively; P < 0.025). After vasopressin was given at minute 8 during CPR, mean ± SEM coronary perfusion pressure was significantly higher in the ACD + ITV group, but did not increase in the STD group (29 ± 3 versus 15 ± 2 mm Hg, and 25 ± 1 versus 14 ± 1 mm Hg at minute 12 and 18, respectively; P < 0.001); mean ± SEM common carotid blood flow remained higher at respective time points (33 ± 8 versus 10 ± 3 mL/min, and 31 ± 7 versus 7 ± 3 mL/min, respectively; P < 0.01). Without active rewarming, spontaneous circulation was restored and maintained for 1 h in three of seven animals in the ACD + ITV group versus none of seven animals in the STD CPR group (not significant). During hypothermic cardiac arrest, ACD CPR with the ITV improved common carotid blood flow compared with STD CPR alone. Moreover, after the administration of vasopressin, coronary perfusion pressure was significantly higher during ACD + ITV CPR, but not during STD CPR.

New strategies are needed to improve the efficiency of cardiopulmonary resuscitation (CPR) in hypothermic cardiac arrest. Active compression-decompression CPR with the inspiratory threshold valve improved carotid blood flow (and coronary perfusion pressure with vasopressin) compared with standard CPR.

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