Abstract:Background
The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung.
Methods
Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; pla… Show more
“…Indeed, the effects of respiratory rate on VILI have been described in experimental animals (27,28). In particular, when we applied a strain greater than 2, which invariably leads to death when delivered at a rate of 15 bpm, we found a lack of injurious effect if delivered at 3 or 6 bpm (29). The relevance of respiratory rate underlines another possible scenario: indeed, in analogy with materials fatigue, it may be possible that damage occurs only after a given number of stress and strain cycles have been delivered and generated into the lung (i.e., VILI below the stress at rupture requires time).…”
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 1.12Ă10 -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.
“…Indeed, the effects of respiratory rate on VILI have been described in experimental animals (27,28). In particular, when we applied a strain greater than 2, which invariably leads to death when delivered at a rate of 15 bpm, we found a lack of injurious effect if delivered at 3 or 6 bpm (29). The relevance of respiratory rate underlines another possible scenario: indeed, in analogy with materials fatigue, it may be possible that damage occurs only after a given number of stress and strain cycles have been delivered and generated into the lung (i.e., VILI below the stress at rupture requires time).…”
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 1.12Ă10 -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.
“…Nevertheless, only a single respiratory cycle is measured when performing this calculation. To ascertain what happens over a longer period, power (energy multiplied by respiratory rate) is measured instead [22]. In this line, a recent study reported that VILI may develop if mechanical power exceeds 12 J/min.…”
“…As a concept, the less you transfer energy to the injured lungs, the better it is. Even if this concept is mainly established in animal model (10), there are some arguments in a recent second analysis of the two randomized clinical trials PROSEVA and ACURASY of the impact of mechanical power on prognosis (11).…”
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