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Current Protective Ventilation Approach

  • Gary F. Nieman,
  • Nader M. Habashi

摘要

The current strategy aimed at mitigating ventilator-induced lung injury (VILI) in patients with or at high risk of developing acute respiratory distress syndrome (ARDS) involves reducing tidal volume (VT) and plateau pressure (Pplat) while adjusting the fraction of inspired oxygen (FiO2) and positive end-expiratory pressure (PEEP) using the ARDSnet low VT (LVT) method (The Acute Respiratory Distress Syndrome Network, N Engl J Med 342:1301–8, 2000). This approach is grounded in the two-compartment model of ARDS pathology, which delineates (i) a small amount of normal lung tissue in the nondependent compartment, often referred to as the “baby lung” and (ii) injured, unstable, collapsed, and edematous tissue in the dependent compartment (Gattinoni and Pesenti, Intensive Care Med 31:776–84, 2005). The proposed two-compartment model suggests that the reduction in end-expiratory lung volume (EELV) due to tissue collapse, coupled with low lung compliance in the dependent compartment, significantly diminishes the availability of normal lung tissue for ventilation. Consequently, it was hypothesized that a primary mechanism of VILI is the overdistension of the compliant normal “baby lung.” This scenario is postulated to occur when the remaining healthy lung tissue is ventilated with a standard-size VT (Gattinoni and Pesenti, Intensive Care Med 31:776–84, 2005; Gattinoni et al., Am Rev Respir Dis 136:730–6, 1987). However, recent evidence challenges the two-compartment model, proposing that pathophysiological changes driving VILI involve regional alveolar instability and collapse scattered throughout the lung, even in nondependent tissue (i.e., the baby lung) appearing normal on chest X-ray or CT scan. Regional alveolar instability induces atelectrauma, while regional collapse generates stress multipliers, concentrating stress and strain in the surrounding normal alveoli, leading to both atelectrauma and volutrauma. This chapter reviews the physiological concepts of safeguarding the baby lung from overdistension using LVT as a protective ventilation strategy.