• Geoffrey P Dobson and Yulia Djabir.
• Department of Physiology and Pharmacology, Heart and Trauma Research Laboratory, James Cook University, Queensland 4811, Australia.
• Am J Emerg Med. 2013 Nov 1;31(11):1539-45.

IntroductionSudden cardiac death generally arises from either ventricular fibrillation or asphyxial hypoxia. In an effort to translate the cardioprotective effects of adenosine and lidocaine (AL) from hemorrhagic shock to cardiopulmonary resuscitation, we examined the effect of AL on hemodynamics and electrocardiogram (ECG) stability in the rat model of asphyxial hypoxia.MethodsMale Sprague-Dawley rats were randomly assigned to 1 of 4 groups (n = 8): saline (SAL), adenosine (ADO), lidocaine (LIDO), and AL. Cardiac arrest (mean arterial pressure <10 mm Hg) was induced by clamping the ventilator line for 8 minutes. A 0.5-mL intravenous drug bolus was injected followed by chest compressions (300 min(-1)), which were repeated every 5 minutes for 1 hour.ResultsReturn of spontaneous circulation was achieved in 5 SAL (62.6%), 4 ADO (50%), 7 LIDO (87.5%), and 8 AL rats (100%) within 5 minutes but could not be sustained. During chest compressions, mean arterial pressure was consistently higher in the AL-treated rats compared with all groups (P < .05; 35-45 and 55 minutes) followed by the LIDO group and was lowest in the ADO and SAL groups (P < .05). Systolic pressure followed a similar pattern. In addition, diastolic pressure in the AL-treated rats was significantly higher from 25 to 60 minutes than LIDO and ADO alone or SAL, and heart rate was 30% to 40% lower. Improved ECG rhythm and R-R variability were apparent in AL-treated rats during early compressions and hands-off intervals.ConclusionsWe conclude that a small bolus of 0.9% NaCl AL improved hemodynamics with possible diastolic rescue and ECG stabilization during chest compressions compared with ADO, LIDO, or SAL controls.Copyright © 2013 Elsevier Inc. All rights reserved.

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