Abstract

BackgroundVeno-arterial extracorporeal membrane oxygenation (ECMO-CPR) is a life-saving rescue for selected patients when standard cardiopulmonary resuscitation fails. The use is increasing although the treatment modality is not fully established. Resuscitated patients typically develop a detrimental early post-arrest cardiac dysfunction that also deserves main emphasis. The present study investigates an ECMO-CPR strategy in pigs and assesses early post-arrest left ventricular function in detail. We hypothesised that a significant dysfunction could be demonstrated with this model using magnetic resonance imaging (MRI), not previously used early post-arrest.MethodsIn eight anaesthetised pigs, a 15-min ventricular fibrillation was resuscitated by an ECMO-CPR strategy of 150-min veno-arterial ECMO aiming at high blood flow rate and pharmacologically sustained aortic blood pressure and pulse pressure of 50 and 15 mmHg, respectively. Pre-arrest cardiac MRI and haemodynamic measurements of left ventricular function were compared to measurements performed 300-min post-arrest.ResultsAll animals were successfully resuscitated, weaned from the ECMO circuit, and haemodynamically stabilised post-arrest. Cardiac output was maintained by an increased heart rate post-arrest, but left ventricular ejection fraction and stroke volume were decreased by approximately 50 %. Systolic circumferential strain and mitral annular plane systolic excursion as well as the left ventricular wall thickening were reduced by approximately 50–70 % post-arrest. The diastolic function variables measured were unchanged.ConclusionsThe present animal study demonstrates a successful ECMO-CPR strategy resuscitating long-lasting cardiac arrest with adequate post-arrest haemodynamic stability. The associated severe systolic left ventricular dysfunction could be charted in detail by MRI, a valuable tool for future cardiac outcome assessments in resuscitation research.Trial registrationInstitutional protocol number: FOTS 4611/13.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-015-0061-2) contains supplementary material, which is available to authorized users.

Highlights

  • Veno-arterial extracorporeal membrane oxygenation (ECMO-CPR) is a life-saving rescue for selected patients when standard cardiopulmonary resuscitation fails

  • Patients with cardiac arrest not responding to standard cardiopulmonary resuscitation (CPR) can be resuscitated by veno-arterial extracorporeal membrane oxygenation (ECMO-CPR)

  • The 15 min duration of cardiac arrest followed by ECMO-CPR was chosen to allow early survival [23, 27,28,29,30], but with a significant post-arrest cardiac dysfunction that could be examined by cardiac magnetic resonance imaging (MRI) in a stable state

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Summary

Introduction

Veno-arterial extracorporeal membrane oxygenation (ECMO-CPR) is a life-saving rescue for selected patients when standard cardiopulmonary resuscitation fails. Resuscitated patients typically develop a detrimental early post-arrest cardiac dysfunction that deserves main emphasis. The present study investigates an ECMO-CPR strategy in pigs and assesses early post-arrest left ventricular function in detail. We hypothesised that a significant dysfunction could be demonstrated with this model using magnetic resonance imaging (MRI), not previously used early post-arrest. A clinical problem after ROSC, is the early post-arrest cardiac dysfunction with circulatory failure-increasing the risk of adverse neurological function and poor outcome in resuscitated patients [9]. The purpose of the present study was twofold; (1) to investigate ECMO-CPR in an experimental pig model and (2) to assess the early post-arrest left ventricular (LV) function by cardiac magnetic resonance imaging (MRI). We hypothesised that a significant early post-arrest LV dysfunction could be demonstrated with this model using MRI. Cardiac MRI allows accurate measurements of motions, volumes and flow in the beating heart and is not previously used to describe early post-arrest cardiac dysfunction

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