Lung anatomy, energy load, and ventilator-induced lung injury

Protti, Alessandro; Andreis, Davide T.; Milesi, M.; Iapichino, G.; Monti, Massimo; Comini, Beatrice; Pugni, Paola; Melis, Valentina; Santini, Alessandro; Dondossola, Daniele; Gatti, Stefano; Lombardi, Luciano; Votta, Emiliano; Carlesso, Eleonora; Gattinoni, Luciano

doi:10.1186/s40635-015-0070-1

Cited by 80 publications

(74 citation statements)

References 51 publications

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“…This underlines how, when tidal volume is added to PEEP volume, it becomes extremely easy to overcome the TLC limits, at which the extracellular matrix is at risk of micro-fractures or rupture. See also Protti et al (36). PEEP, positive end-expiratory pressure; ARDS, acute respiratory distress syndrome; TLC, total lung capacity.…”

Section: Peep and Oxygenationmentioning

confidence: 99%

Positive end-expiratory pressure: how to set it at the individual level

Gattinoni¹,

Collino²,

Maiolo³

et al. 2017

Ann. Transl. Med.

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Abstract:The positive end-expiratory pressure (PEEP), since its introduction in the treatment of acute respiratory failure, up to the 1980s was uniquely aimed to provide a viable oxygenation. Since the first application, a large debate about the criteria for selecting the PEEP levels arose within the scientific community. Lung mechanics, oxygen transport, venous admixture thresholds were all proposed, leading to PEEP recommendations from 5 up to 25 cmH 2 O. Throughout this period, the main concern was the hemodynamics. This paradigm changed during the 1980s after the wide acceptance of atelectrauma as one of the leading causes of ventilator induced lung injury. Accordingly, the PEEP aim shifted from oxygenation to lung protection. In this framework, the prevention of lung opening and closing became an almost unquestioned dogma. Consequently, as PEEP keeps open the pulmonary units opened during the previous inspiratory phase, new methods were designed to identify the 'optimal' PEEP during the expiratory phase.The open lung approach requires that every collapsed unit potentially openable is opened and maintained open. The methods to assess the recruitment are based on imaging (computed tomography, electric impedance tomography, ultrasound) or mechanically-driven gas exchange modifications. All the latest assume that whatever change in respiratory system compliance is due to changes in lung compliance, which in turn is uniquely function of the recruitment. Comparative studies, however, showed that the only possible approach to measure the amount of collapsed tissue regaining inflation is the CT scan. In fact, all the other methods estimate as recruitment the gas entry in pulmonary units already open at lower PEEP, but increasing their compliance at higher PEEP. Since higher PEEP is usually more indicated (also for oxygenation) when the recruitability is higher, as occurs with increasing severity, a meaningful PEEP selection requires the assessment of recruitment. The Berlin definition may help in this assessment.

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Section: Peep and Oxygenationmentioning

confidence: 99%

Positive end-expiratory pressure: how to set it at the individual level

Gattinoni¹,

Collino²,

Maiolo³

et al. 2017

Ann. Transl. Med.

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“…What matters, however, is the slope of such relationship, which equals the ratio of lung elastance to total respiratory system elastance (E L /E tot ), which averages 0.7 in the population, but ranges from 0.2 to 0.8 (16). If we consider as a possible threshold for VILI a value of transpulmonary pressure at which some of the pulmonary units are fully inflated (i.e., in which the collagen fibers of the extracellular matrix are completely distended), a reference value of 21 cmH 2 O may be experimentally identified (17). In an average patient (E L / E tot =0.7), this transpulmonary pressure value would equate to 30 cmH 2 O airway pressure.…”

Section: Pressurementioning

confidence: 99%

Driving pressure and mechanical power: new targets for VILI prevention

et al. 2017

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Several factors have been recognized as possible triggers of ventilator-induced lung injury (VILI).The first is pressure (thus the 'barotrauma'), then the volume (hence the 'volutrauma'), finally the cyclic opening-closing of the lung units ('atelectrauma'). Less attention has been paid to the respiratory rate and the flow, although both theoretical considerations and experimental evidence attribute them a significant role in the generation of VILI. The initial injury to the lung parenchyma is necessarily mechanical and it could manifest as an unphysiological distortion of the extracellular matrix and/or as micro-fractures in the hyaluronan, likely the most fragile polymer embedded in the matrix. The order of magnitude of the energy required to break a molecular bond between the hyaluronan and the associated protein is 1.12×10 -16 Joules (J), 70-90% higher than the average energy delivered by a single breath of 1L assuming a lung elastance of 10 cmH 2 O/L (0.5 J). With a normal statistical distribution of the bond strength some polymers will be exposed each cycle to an energy large enough to rupture. Both the extracellular matrix distortion and the polymer fractures lead to inflammatory increase of capillary permeability with edema if a pulmonary blood flow is sufficient. The mediation analysis of higher vs. lower tidal volume and PEEP studies suggests that the driving pressure, more than tidal volume, is the best predictor of VILI, as inferred by increased mortality. This is not surprising, as both tidal volume and respiratory system elastance (resulting in driving pressure) may independently contribute to the mortality. For the same elastance driving pressure is a predictor similar to plateau pressure or tidal volume. Driving pressure is one of the components of the mechanical power, which also includes respiratory rate, flow and PEEP. Finding the threshold for mechanical power would greatly simplify assessment and prevention of VILI.

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“…To this end, Gattinoni's group recently published two papers using an engineering analysis to determine the impact of the mechanical breath on the lung injury (16,17). They demonstrated that the applied stress, which for the lung is the Vt, impacts: (I) lung anatomy resulting in either collapse and heterogeneity or recruitment and homogeneous ventilation; (II) the energy load placed upon the lung and (III) dynamic strain (e.g., the change in lung size and shape in response to the applied stress) on lung tissue.…”

mentioning

confidence: 99%

“…However, if the lower limit of inspiratory capacity was reached, but not exceeded, excessive dynamic strain (high Vt plus low PEEP) caused VILI, whereas a high static strain (low Vt plus high PEEP) did not (16). In addition, Protti et al showed that PEEP was lung protective as long as it was associated with reduced Vt, increasing static strain but reducing dynamic strain (17).…”

mentioning

confidence: 99%