• James T Niemann and Daniel Garner.
• Department of Emergency Medicine, Harbor-UCLA Medical Center, 1000 West Carson Street, Box 21, Torrance, CA 90509, USA. jniemann@emedharbor.edu
• Resuscitation. 2005 Apr 1;65(1):97-101.

ObjectiveA dramatic increase in plasma catecholamines has been demonstrated consistently following cardiac arrest and during CPR. The time course of this initial catecholamine surge after successful resuscitation has not been well studied. The purpose of this study was to measure plasma catecholamines after successful resuscitation and to determine their relationship to post-resuscitation hemodynamics.MethodsVF cardiac arrest was induced in eight anesthetized and instrumented swine. After 5 min of VF, conventional CPR was initiated followed 2 min later by transthoracic defibrillation. Restoration of spontaneous circulation (ROSC) was achieved in six animals. Following resuscitation, hemodynamic variables and plasma catecholamines were measured at intervals.ResultsMyocardial contractility (peak systolic dP/dt), stoke volume, left ventricular stroke work (LVSW), and mean arterial pressure (MAP) were significantly decreased from pre-arrest values within 15 min of ROSC and remained depressed during 60 min of observation. Systemic vascular resistance (SVR) was significantly increased within 15 min and remained elevated. Significant negative correlations were observed between SVR and plasma epinephrine (adrenaline) (r=-0.72, p<0.001) and norepinephrine (noradrenaline) (r=-0.76, p<0.001). Significant negative correlations were also observed between MAP and these catecholamines. A negative correlation was also observed between norepinephrine and LVSW (r=-0.50, p=0.039). Catecholamine levels were not related to other indices of cardiac function.ConclusionsA post-resuscitation adrenergic state is driven by a decline in MAP and PVR. Although seemingly compensatory, it may also contribute to the observed decline in cardiac function.

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