The targets of mechanical ventilation in ARDS have shifted from providing normal gas exchange to protecting the lung from VILI. The distending force of the lung (the trigger of VILI) is the transpulmonary pressure (PL)—the difference between the airway pressure (Paw) and the pleural pressure. For the same driving force, in normal conditions, the transpulmonary pressure equals the driving force multiplied by the ratio between the lung elastance and the respiratory system elastance (lung elastance + chest wall elastance): PL = Paw * EL/ETOT. In normal subjects, this ratio is approximately 0.5; in ARDS patients, it may be 0.2 to 0.8. Consequently, the airway pressure alone may be misleading to assess the transpulmonary pressure imposed on the lung by mechanical ventilation (i.e., to assess the stress). We used airway pressure to indicate end inspiratory pressure. The delivered tidal volume increases the lung volume and in the process produces strain on the lung. The ratio of change in lung volume over resting lung volume (ΔV/V0) is a rough approximation of the strain. Excessive strain causes shape changes of endothelial and epithelial cells inducing an inflammatory reaction. Because the resting volume (V0, the baby lung) may vary largely in ARDS, the same tidal volume per ideal body weight may induce largely different strain values. Stress and strain, the triggers of VILI, are linked by a constant, specific lung elastance (Espec), accounting for the following relationship: PL (stress) = Espec * ΔV/V0 (strain). The specific lung elastance is similar in normal subjects and in ARDS patients. Physiologic variables are generally poor indicators of the severity of lung injury, with the alveolar deadspace being the only variable associated with outcome. The severity of lung injury may be assessed by CT scan. The fraction of nonaerated lung tissue is strongly associated with mortality. The greater the lung injury, the smaller the baby lung, and the greater the stress-strain induced by mechanical ventilation. Among outcome studies testing different tidal volumes, only the study comparing the two extreme values tested (6 mL/kg versus 12 mL/kg) showed a significant benefit of lower tidal volume. Data from clinical studies and rationale from physiologic studies are strongly in favor of using the lowest tidal volume possible, likely associated with lower stress and strain, accepting hypercapnia as a side effect. All studies comparing lower versus higher PEEP randomly applied to unselected ARDS populations failed to show benefits on survival. In contrast, benefits of higher PEEP were found in more severe selected ARDS patients. The lung recruitability may vary greatly within the ARDS population (5% to 50% of the lung parenchyma) and is correlated with the overall lung injury severity. Higher PEEP possibly should be reserved only for patients with higher recruitability. When treating patients with ARDS, individual characteristics (lung injury severity, gas exchange, lung mechanics, abdominal pressure) should be assessed to tailor the least harmful mechanical ventilation according to the available evidence and physiologic rationale, providing the lowest stress and strain possible. In the severe ARDS were mechanical ventilation is more harmful associated therapy as prone positioning and extra-corporeal support must be sought on.
ICM experimental 2: what have I learnt from experimental physiology / L. Gattinoni. ((Intervento presentato al 28. convegno ESICM LIVES tenutosi a Berlin nel 2015.
|Titolo:||ICM experimental 2: what have I learnt from experimental physiology|
GATTINONI, LUCIANO (Primo)
|Data di pubblicazione:||6-ott-2015|
|Settore Scientifico Disciplinare:||Settore MED/41 - Anestesiologia|
|Citazione:||ICM experimental 2: what have I learnt from experimental physiology / L. Gattinoni. ((Intervento presentato al 28. convegno ESICM LIVES tenutosi a Berlin nel 2015.|
|Appare nelle tipologie:||14 - Intervento a convegno non pubblicato|