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Publications

Journal Article Ahead of print

PubMed: 42168794 DOI: 10.1111/aor.70163

Comparison of Left Ventricular Pressure-Volume Loops With Veno-Arterial Extracorporeal Membrane Oxygenator Support: In Vitro Investigation.

Artif Organs

Authors: Eric L Wu, Johannes Boesch, Hideaki Nonaka, Christopher Djelovic, Avishka Wickramarachchi, Jessica Benitez, John F Fraser

Affiliations

  • Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group, The Prince Charles Hospital, Chermside, Australia.
  • Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia.
  • School of Mechanical and Mining Engineering, The University of Queensland, Brisbane, Australia.
  • Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group, The Prince Charles Hospital, Chermside, Australia. Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia. Department of Anaesthesia and Intensive Care Medicine, Medical University Innsbruck, Innsbruck, Austria.
  • Advanced Cardiorespiratory Engineering Laboratory (ACElab), School of Mechanical, Medical and Process Engineering, Centre for Biomedical Technologies, Queensland University of Technology, Brisbane, Australia.
  • Innovative Cardiovascular Engineering and Technology Laboratory (ICETLab), Critical Care Research Group, The Prince Charles Hospital, Chermside, Australia. Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia.

Abstract

BACKGROUND

The hemodynamic consequence of increasing veno-arterial extracorporeal membrane oxygenator (V-A ECMO) flow on left ventricular (LV) loading is controversial, with in vivo studies reporting conflicting results on left ventricular distension. We investigated increased V-A ECMO flow on LV pressure-volume characteristics under varying cardiac and volume conditions using a repeatable in vitro mock circulation loop (MCL).

METHODS

A MCL was configured with V-A ECMO system to simulate four cardiogenic shock patients due to decompensated chronic heart failure patient: (1) LV failure with healthy right ventricle (RV) at normal volume (mean circulatory filling pressure, MCFP: 7 mmHg), (2) combined LV and RV failure at normal volume, (3) LV failure with healthy RV and volume overload (MCFP: 12 mmHg), and (4) combined LV and RV failure with volume overload. For each condition, ECMO flow was increased from 2 L/min to 4 L/min, and systemic vascular resistance (SVR) was adjusted to evaluate effects on LV pressure-volume loops.

RESULTS

In LV failure with preserved RV function with normal volume, increased ECMO flow at constant SVR led to LV distension (> 30 mL increase in end-diastolic volume). Reducing SVR mitigated this effect but resulted in hypotension (MAP < 65 mmHg). In combined LV and RV failure at normal volume, LV distension was less pronounced and manageable with SVR reduction while maintaining adequate MAP. Under volume overload, ECMO flow increases caused marked LV dilation and elevated central venous pressure, risking venous congestion.

CONCLUSIONS

We demonstrated that LV distension during V-A ECMO flow is influenced by ventricular function, volume status, and SVR. Judicious volume management and afterload control are essential, and patients with preserved RV function may require adjunct LV unloading strategies.

MeSH

Oxygenators, Ventricular Pressure, Oxygenators, Membrane, Membranes