Abstract
BackgroundPositive-pressure mechanical ventilation is an essential therapeutic intervention, yet it causes the clinical syndrome known as ventilator-induced lung injury. Various lung protective mechanical ventilation strategies have attempted to reduce or prevent ventilator-induced lung injury but few modalities have proven effective. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury.ObjectivesTo evaluate the effects of positive end-expiratory pressure and recruitment maneuvers in reducing lung injury in a ventilator-induced lung injury murine model in short- and longer-term ventilation.Methods5–12 week-old female BALB/c mice (n = 85) were anesthetized, placed on mechanical ventilation for either 2 hrs or 4 hrs with either low tidal volume (8 ml/kg) or high tidal volume (15 ml/kg) with or without positive end-expiratory pressure and recruitment maneuvers.ResultsAlteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation. Standardized histology scores, influx of bronchoalveolar lavage albumin, proinflammatory cytokines, and absolute neutrophils were significantly higher in the high-tidal volume ventilation group at 4 hours of ventilation. Application of positive end-expiratory pressure resulted in significantly decreased standardized histology scores and bronchoalveolar absolute neutrophil counts at low- and high-tidal volume ventilation, respectively. Recruitment maneuvers were essential to maintain pulmonary compliance at both 2 and 4 hrs of ventilation.ConclusionsSigns of ventilator-induced lung injury are evident soon after high tidal volume ventilation (as early as 2 hours) and lung injury worsens with longer-term ventilation (4 hrs). Application of positive end-expiratory pressure and recruitment maneuvers are protective against worsening VILI across all time points. Dynamic compliance can be used guide the frequency of recruitment maneuvers to help ameloriate ventilator-induced lung injury.
Highlights
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have a reported mortality rate of 35 to 65% depending on the cohort studied.[1,2] Positive-pressure mechanical ventilation, life-saving, can worsen lung injury and cause the clinical syndrome known as ventilator-induced lung injury.[3,4] Ventilator-induced lung injury (VILI) results from overdistension of the lung parenchyma known as volutrauma, repetitive collapse and reexpansion of alveoli leading to atelectrauma, or both
Alteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation
Signs of ventilator-induced lung injury are evident soon after high tidal volume ventilation and lung injury worsens with longer-term ventilation (4 hrs)
Summary
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) have a reported mortality rate of 35 to 65% depending on the cohort studied.[1,2] Positive-pressure mechanical ventilation, life-saving, can worsen lung injury and cause the clinical syndrome known as ventilator-induced lung injury.[3,4] Ventilator-induced lung injury (VILI) results from overdistension of the lung parenchyma known as volutrauma, repetitive collapse and reexpansion of alveoli leading to atelectrauma, or both This mechanical stretch induces the release of inflammatory mediators, or biotrauma, perpetuating this injury.[5] VILI has received increasing attention because a strategy to limit tidal stretch improved outcomes in ARDS and reduction in tidal volume ventilation resulted in a dramatic improvement in mortality rates in acute lung injury and acute respiratory distress syndrome.[2,6]. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury
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