Adaptive Support Ventilation Attenuates Ventilator Induced Lung Injury: Human and Animal Study.

Dai Dai,Chang Chang,Yang Yang,Huang Huang,Wu Wu,Peng Peng

doi:10.3390/ijms20235848

Abstract

Adaptive support ventilation (ASV) is a closed-loop ventilation, which can make automatic adjustments in tidal volume (VT) and respiratory rate based on the minimal work of breathing. The purpose of this research was to study whether ASV can provide a protective ventilation pattern to decrease the risk of ventilator-induced lung injury in patients of acute respiratory distress syndrome (ARDS). In the clinical study, 15 ARDS patients were randomly allocated to an ASV group or a pressure-control ventilation (PCV) group. There was no significant difference in the mortality rate and respiratory parameters between these two groups, suggesting the feasible use of ASV in ARDS. In animal experiments of 18 piglets, the ASV group had a lower alveolar strain compared with the volume-control ventilation (VCV) group. The ASV group exhibited less lung injury and greater alveolar fluid clearance compared with the VCV group. Tissue analysis showed lower expression of matrix metalloproteinase 9 and higher expression of claudin-4 and occludin in the ASV group than in the VCV group. In conclusion, the ASV mode is capable of providing ventilation pattern fitting into the lung-protecting strategy; this study suggests that ASV mode may effectively reduce the risk or severity of ventilator-associated lung injury in animal models.

Highlights

Acute respiratory distress syndrome (ARDS) has been studied for more than 50 years since its identification by Ashbaugh in 1967 [1]
The patients were assigned to the Adaptive support ventilation (ASV) group or pressure-control ventilation (PCV) group according to treatment
Our results showed that the ASV mode was able to control the VT in the range of 6–8 mL/kg IBW in most ARDS patients, suggesting highly feasible to apply this mode as part of the lung-protective ventilation strategy

Summary

Introduction

Acute respiratory distress syndrome (ARDS) has been studied for more than 50 years since its identification by Ashbaugh in 1967 [1]. Neutrophil mobilization and activity increase, and hyaline membranes accumulate, which triggers simultaneous alveolar hemorrhage and edema, which in turn increase the pulmonary dead space and cause intrapulmonary shunting [2,3]. These events impair lung compliance and oxygenation, and generate respiratory distress symptoms. Another study has reported an association between mechanical ventilation and damage to the extracellular matrix (ECM) in alveolar epithelial cells [8]. These findings suggest that it may be possible to reduce the risk or severity of VILI by understanding the influence of ventilation mode on alveolar epithelial cells

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Conclusion