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Updated: Sep 26, 2026

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
Published on: April 7, 2021
Physiologic rationale for ventilator setting in acute lung injury/acute respiratory distress syndrome patients
Luciano Gattinoni1, Federica Vagginelli, Davide Chiumello
1Istituto di Anestesia e Rianimazione, Universita' degli Studi di Milano, Ospedale Policlinico-IRCCS, Milano, Italy.
Objectives:
To review the physiologic approach to setting mechanical ventilation in acute lung injury/acute respiratory distress syndrome.
Data Sources:
MEDLINE search from 1979 to the present.
Data Selection:
Personal selection of some articles we believe relevant for understanding acute lung injury/acute respiratory distress syndrome physiopathology and its physiologic management.
Data Summary:
Knowing the underlying pathology is key to estimating the potential for recruitment. The potential for recruitment is rather low when the consolidation of pulmonary units exceeds collapse, as in diffuse pneumonia. In contrast, when pulmonary unit collapse exceeds consolidation, as in acute lung injury/acute respiratory distress syndrome from extrapulmonary origin, the potential for recruitment may be high. To exploit the potential for recruitment, a transpulmonary pressure greater than the opening pressure must be applied to the lung. To do so, chest wall elastance must be measured or estimated. To avoid collapse after recruitment, a positive end-expiratory pressure greater than the compressive forces operating on the lung and an alveolar ventilation sufficient to prevent absorption atelectasis must be provided. Indeed, avoidance of stretch (low airway plateau pressure) and prevention of cyclic collapse and reopening (adequate positive end-expiratory pressure and alveolar ventilation) are the physiologic cornerstones of mechanical ventilation in acute lung injury/acute respiratory distress syndrome. When considering all the randomized clinical trials reported so far, it is tempting to speculate that transpulmonary pressure and stresses, rather than tidal volume per se, are the key factors that may have an impact on mortality.
Conclusions:
The majority of physiologic, experimental, and clinical trial data converge on one simple concept: treat the lung gently.
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