Elsevier

Resuscitation

Volume 64, Issue 2, February 2005, Pages 227-232
Resuscitation

Influence of dobutamine on the variables of systemic haemodynamics, metabolism, and intestinal perfusion after cardiopulmonary resuscitation in the rat

https://doi.org/10.1016/j.resuscitation.2004.08.003Get rights and content

Abstract

Background:

Global left ventricular dysfunction after successful resuscitation from cardiac arrest may be treated successfully with dobutamine but the effects on intestinal perfusion are unknown.

Methods:

In 24 male Sprague-Dawley rats ventricular fibrillation was induced. After 4 min of untreated cardiac arrest, precordial chest compression was performed for 4 min; adrenaline (epinephrine) (90 μg kg–1) was injected, followed by defibrillation. Return of spontaneous circulation was achieved in 18 animals, which were allocated to receive saline 0.9% (control group, n = 6), dobutamine at 5 μg kg–1 min–1 (n = 6) or dobutamine at 10 μg kg–1 min–1 (n = 6). Measurements of haemodynamic variables and intestinal tonometer PCO2 were made before induction of ventricular fibrillation and 15, 30, 60, and 120 min postresuscitation.

Results:

At 120 min postresuscitation, mean aortic pressure was 82 ± 20, 104 ± 19, and 113 ± 15 mmHg for the control group, the dobutamine (5 μg kg–1 min–1) group and the dobutamine (10 μg kg–1 min–1) group (P < 0.05 for comparison of the dobutamine (10 μg kg–1 min–1) group versus the control group). Respective abdominal aortic blood flow was 107 ± 16, 133 ± 49, and 145 ± 18 ml min–1 kg–1 (P < 0.05 for comparison of the dobutamine (10 μg kg–1 min–1) group versus the control group), and superior mesenteric artery blood flow was 25 ± 9, 28 ± 8, and 33 ± 8 ml min–1 kg–1. Arterial lactate was significantly higher (P < 0.05) in the control group (2.3 ± 0.6 mmol l–1) than in the dobutamine (5 μg kg–1 min–1) group (1.6 ± 0.3 mmol l–1) and dobutamine (10 μg kg–1 min–1) group (1.5 ± 0.3 mmol l–1). Tonometrically derived PCO2 gap was highly elevated at 15 min of postresuscitation and returned to prearrest level at 120 min postresuscitation in all groups.

Conclusions:

Dobutamine enhances the recovery of global haemodynamic and metabolic variables early after cardiac arrest.

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 PCO2, 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.

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