At zero flow, airway and alveolar pressure are equal, for example during an end-inspiratory plateau pressure maneuver. Transpulmonary pressure (P airway − P pleural) is the pertinent distending pressure of the lung. 11– 13 Comparable transpulmonary pressures are achieved for a given lung volume regardless of whether airway pressure is positive (as during mechanical ventilation) or negative (as during normal spontaneous breathing). Yet, the pertinent distending pressure of the lungs is not simply the airway pressure, but rather the transpulmonary pressure (airway minus pleural pressure), the difference between the pressure inside versus outside the lung ( Fig. It is true that high airway pressure per se does not cause VILI, as these studies confirmed. Similar findings have been replicated in other animal models, 7– 9 leading to the misleading conclusion that volutrauma is more important than barotrauma. Animals supported with either high-volume strategy had markedly more severe lung injury compared to animals ventilated with the high-pressure low-volume strategy. Conversely, the low-pressure high-volume strategy was achieved via an iron lung (negative pressure ventilator). The high-pressure low-volume strategy was achieved via thoracoabdominal strapping with rubber bands, decreasing chest wall compliance. In a classic study by Dreyfuss et al., 6 rats were mechanically ventilated using one of three strategies: (1) high airway pressures and high tidal volumes (2) high airway pressures and low tidal volumes or (3) low airway pressures and high tidal volumes. Lung injury caused by alveolar overdistension.įor much of the last thirty years, barotrauma (high inflation pressure-mediated lung injury) and volutrauma (overdistension-mediated lung injury) were viewed as distinct albeit related entities. Pressure difference inside versus outside the lung (P TP = P airway − P pleural), which is the pertinent distending pressure of the lung.Īirway and alveolar pressure are equal at points of zero-flow. Stress is represented by the transpulmonary pressure. Internal forces per unit area that balance an external load. Ventilated patient is controversial because ideal resting size/shape Calculation of lung strain in the mechanically Shear strain would produce an oblique-angled rhombus.Ĭhange in size/shape of an object relative to its resting size/shape,Įxpressed as ratio of displacement magnitude divided by As example, if resting object is square-shaped, Well-aerated lung adjacent to patchy ground-glass opacities andĪngular deformation of an object relative to its restingĬonformation. Interdependent interalveolar septae shared between aeratedĪlveoli and adjacent fluid-filled or atelectatic alveoli. Lung and chest wall, and is often incorrectly labeled as lungĬhange in pressure for a given change in volume, also calledĭifferences in regional lung mechanics owing to mechanically Respiratory system compliance reflects contributions of both the (ΔV/ΔP transpulmonary), or chest wall compliance (ΔV/ΔP pleural). Respiratory system compliance (ΔV/ΔP airway), lung compliance Injurious inflammatory response to mechanical lung injury.Ĭhange in volume for a given change in pressure. forceful inspiratory effort).Īdditional lung and extra-pulmonary organ injury caused by pro. May occurĮven at lower airway pressure if pleural pressure is extremely Lung injury caused by high transpulmonary pressure. Lung injury caused by high shear forces from cyclic opening andĬollapse of atelectatic but recruitable lung units.Ĭonceptual model for the reduced volume of non-atelectaticĪerated lung available for tidal insufflation and gas exchange in 4 Recent recognition that heterogeneous regional mechanics, stress frequency, and pulmonary capillary stress failure may also contribute to VILI has inspired a renewed line of investigation toward personalizing lung-protective ventilation. 3Ĭlassically, four mechanisms of VILI have been described: barotrauma, volutrauma, atelectrauma, and biotrauma ( Table 1). 1 Over 250 years later, ventilator-induced lung injury (VILI) was proven definitively to contribute to mortality in patients with acute respiratory distress syndrome (ARDS). 1, 2 John Fothergill postulated mouth-to-mouth resuscitation may be preferable to mechanical ventilation because “the lungs of one man may bear, without injury, as great a force as those of another man can exert which by the bellows cannot always be determined”. The potential for mechanical ventilation to cause harm was first described in the mid-18 th century. As with most medical and pharmacological interventions, mechanical ventilation must be titrated within a therapeutic window, providing the required life-sustaining support while minimizing unintended toxicity.
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