Abstract

BackgroundCardiogenic pulmonary oedema (CPE) may contribute to ventilator-associated lung injury (VALI) in patients with cardiogenic shock. The appropriate ventilatory strategy remains unclear. We aimed to evaluate the impact of ultra-low tidal volume ventilation with tidal volume of 3 ml/kg predicted body weight (PBW) in patients with CPE and veno–arterial extracorporeal membrane oxygenation (V–A ECMO) on lung inflammation compared to conventional ventilation.MethodsA single-centre randomized crossover trial was performed in the Cardiac Intensive Care Unit (ICU) at a tertiary university hospital. Seventeen adults requiring V–A ECMO and mechanical ventilation due to cardiogenic shock were included from February 2017 to December 2018. Patients were ventilated for two consecutive periods of 24 h with tidal volumes of 6 and 3 ml/kg of PBW, respectively, applied in random order. Primary outcome was the change in proinflammatory mediators in bronchoalveolar lavage fluid (BALF) between both ventilatory strategies.ResultsVentilation with 3 ml/kg PBW yielded lower driving pressures and end-expiratory lung volumes. Overall, there were no differences in BALF cytokines. Post hoc analyses revealed that patients with high baseline levels of IL-6 showed statistically significant lower levels of IL-6 and IL-8 during ultra-low tidal volume ventilation. This reduction was significantly proportional to the decrease in driving pressure. In contrast, those with lower IL-6 baseline levels showed a significant increase in these biomarkers.ConclusionsUltra-low tidal volume ventilation in patients with CPE and V–A ECMO may attenuate inflammation in selected cases. VALI may be driven by an interaction between the individual proinflammatory profile and the mechanical load overimposed by the ventilator.Trial registration The trial was registered in ClinicalTrials.gov (identifier NCT03041428, Registration date: 2nd February 2017).

Highlights

  • Cardiogenic pulmonary oedema (CPE) may contribute to ventilator-associated lung injury (VALI) in patients with cardiogenic shock

  • In spite of different pathophysiological mechanisms, alveolar flooding caused by hydrostatic mechanisms in patients with cardiogenic pulmonary oedema (CPE) may produce similar respiratory system mechanics to those observed in patients with acute respiratory distress syndrome (ARDS) [4, 5]

  • Baseline and clinical characteristics of all patients, including causes of cardiogenic shock, according to initial ventilatory strategy are shown in Additional file 2: Table S1

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Summary

Introduction

Cardiogenic pulmonary oedema (CPE) may contribute to ventilator-associated lung injury (VALI) in patients with cardiogenic shock. When end-inspiratory stretch is high or functional residual capacity is low, leading to recruitment/de-recruitment phenomena, excessive mechanical loads may promote tissue damage and inflammation [1]. In patients with the acute respiratory distress syndrome (ARDS), ventilator-associated lung injury (VALI) contributes to lung inflammation and is one major determinant of outcomes [2]. In spite of different pathophysiological mechanisms, alveolar flooding caused by hydrostatic mechanisms in patients with cardiogenic pulmonary oedema (CPE) may produce similar respiratory system mechanics to those observed in patients with ARDS [4, 5]. The effects of this mechanical load on regional inflammation in patients with CPE, in which the inflammatory response may not be so activated as in ARDS, have not been studied

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