Abstract

BackgroundSeptic shock is often associated with acute respiratory distress syndrome, a serious clinical problem exacerbated by improper mechanical ventilation. Ventilator-induced lung injury (VILI) can exacerbate the lung injury caused by acute respiratory distress syndrome, significantly increasing the morbidity and mortality. In this study, we asked the following questions: what is the effect of the lung position (dependent lung versus nondependent lung) on the rate at which VILI occurs in the normal lung? Will positive end-expiratory pressure (PEEP) slow the progression of lung injury in either the dependent lung or the nondependent lung?Materials and methodsSprague–Dawley rats (n = 19) were placed on mechanical ventilation, and the subpleural alveolar mechanics were measured with an in vivo microscope. Animals were placed in the lateral decubitus position, left lung up to measure nondependent alveolar mechanics and left lung down to film dependent alveolar mechanics. Animals were ventilated with a high peak inspiratory pressure of 45 cmH2O and either a low PEEP of 3 cmH2O or a high PEEP of 10 cmH2O for 90 minutes. Animals were separated into four groups based on the lung position and the amount of PEEP: Group I, dependent + low PEEP (n = 5); Group II, nondependent + low PEEP (n = 4);Group III, dependent + high PEEP (n = 5); and Group IV, nondependent + high PEEP (n = 5). Hemodynamic and lung function parameters were recorded concomitant with the filming of alveolar mechanics. Histological assessment was performed at necropsy to determine the presence of lung edema.ResultsVILI occurred earliest (60 min) in Group II. Alveolar instability eventually developed in Groups I and II at 75 minutes. Alveoli in both the high PEEP groups were stable for the entire experiment. There were no significant differences in arterial PO2 or in the degree of edema measured histologically among experimental groups.ConclusionThis open-chest animal model demonstrates that the position of the normal lung (dependent or nondependent) plays a role on the rate of VILI.

Highlights

  • There were no significant differences in arterial PO2 or in the degree of edema measured histologically among experimental groups. This open-chest animal model demonstrates that the position of the normal lung plays a role on the rate of Ventilatorinduced lung injury (VILI)

  • Mechanical ventilation (MV) is essential in the treatment of the acute respiratory distress syndrome (ARDS), but casual MV can lead to a secondary ventilator-induced lung injury (VILI) significantly increasing the morbidity and mortality [1,2,3]

  • The present study clearly demonstrated that alveoli in the low positive end-expiratory pressure (PEEP) group were unstable, and we know from previous studies that alveolar instability leads to VILI if alveoli are unstable for 3–4 hours [5,12]

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Summary

Introduction

Mechanical ventilation (MV) is essential in the treatment of the acute respiratory distress syndrome (ARDS), but casual MV can lead to a secondary ventilator-induced lung injury (VILI) significantly increasing the morbidity and mortality [1,2,3]. Alveolar instability (recruitment/derecruitment) causes a cascade of pathologic events, including a direct mechanical injury to pulmonary tissue that causes a release of cytokines that can exacerbate the systemic inflammatory response syndrome typical of ARDS [6]. Septic shock is often associated with acute respiratory distress syndrome, a serious clinical problem exacerbated by improper mechanical ventilation. Ventilatorinduced lung injury (VILI) can exacerbate the lung injury caused by acute respiratory distress syndrome, significantly increasing the morbidity and mortality. We asked the following questions: what is the effect of the lung position (dependent lung versus nondependent lung) on the rate at which VILI occurs in the normal lung? Will positive end-expiratory pressure (PEEP) slow the progression of lung injury in either the dependent lung or the nondependent lung?

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