Influence of dobutamine on the variables of systemic haemodynamics, metabolism, and intestinal perfusion after cardiopulmonary resuscitation in the rat☆
Introduction
Cardiac arrest, especially in the out-of-hospital setting, carries a grave prognosis, as most victims do not survive [1], [2]. Despite initial success with defibrillation, left ventricular function (LV) is impaired significantly in the postresuscitation period, as shown in humans [3], [4] and in the experimental animal model [5], [6]. Experimentally, the severity of postresuscitation myocardial dysfunction appears to be related to the β-agonistic effects of sympathomimetic amines, which are given during cardiopulmonary resuscitation (CPR) to increase coronary perfusion pressure [7]. Controlled studies performed in pigs have shown that cardiac performance after successful resuscitation with adrenaline followed by defibrillation was characterized by a continuous decline of the LV ejection fraction for the first hours of observation, returning to prearrest values by 48 h postresuscitation [6]. A similar pattern of transient cardiac depression, together with vasodilatation, is reported from survivors of out-of-hospital cardiac arrest [4], whereas non-survivors are characterized by persistently depressed cardiac function. Moreover, a recent study demonstrated “sepsis-like” changes following successful CPR in humans [8], in part similar to those previously described as the postresuscitation visceral syndrome [9]. Experimental [10], [11] and clinical [12], [13] studies have demonstrated mesenteric ischaemia during recovery from various forms of shock, indicated by increased intestinal mucosal , determined tonometrically, and reflecting mucosal acidosis. Intestinal mucosal acidosis and compromised gastrointestinal integrity are known as important risk factors for major complications and outcome in critically ill patients [14], [15].
Experimentally, postresuscitation myocardial dysfunction was prevented by the infusion of dobutamine [16] during the postresuscitation period. As several previous studies show conflicting results with respect to splanchnic perfusion in response to dobutamine, showing vasodilatation [13], minimal effects [17], [18] and vasoconstriction [19], [20], regional intestinal perfusion responses to dobutamine in the postresuscitation setting may not be predicted.
The present prospective study was undertaken to test the hypothesis that dobutamine improves global haemodynamic and regional intestinal perfusion variables after controlled and standardized resuscitation from fibrillatory cardiac arrest.
Section snippets
Materials and methods
The study was approved by the local Animal Care Committee and the procedures complied with the Swiss animal protection laws.
Prearrest
All groups were comparable with respect to all measured variables (Table 1) before induction of VF with the exception of PtCO2, which was slightly, but statistically significantly higher in the dobutamine (5 μg kg–1 min–1) group.
VF and resuscitation
Duration of VF until ROSC was 500 ± 21 s for the control group, 469 ± 49 s for the dobutamine (5 μg kg–1 min–1) group, and 496 ± 16 s for dobutamine (10 μg kg–1 min–1) group (P = 0.21). CPP values during PCC immediately before defibrillation were 44 ± 9, 38 ± 8, and 34 ± 4 mmHg for
Discussion
In this rodent model of VF and CPR, we determined the effects of dobutamine on systemic haemodynamics and intestinal perfusion during the early postresuscitation period following successful resuscitation. The major finding of this study is that MAP and aortic blood flow were elevated by 35% at 120 min postresuscitation with dobutamine infused at 10 μkg–1 min–1, as compared to the control group with no treatment. Together with haemodynamic improvement, arterial lactate was 30% lower than in the
Conflict of interest statement
All authors declare that there are no conflicts of interest regarding the present study.
Acknowledgments
This study is supported by Grant No. 32.40877.94 from the Swiss National Science Foundation. We gratefully acknowledge the editorial help of Bert Drop, MD.
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A Spanish and Portuguese translated version of the Abstract and Keywords of this article appears at 10.1016/j.resuscitation.2004.08.003.