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Background: energy, power, and VILI Repeated applications of tidal energy inflict lung damage (VILI) when stress and strain exceed the limits of tissue tolerance. Inflation work and energy are the products of pressure and volume, which are loosely associated with stress and strain, respectively. Three major pressure components contribute to tidal inflation energy: flow resistive pressure, tidal elastic (driving) pressure, and the static elastic pressure baseline set by PEEP [1, 2]. Although total inflation power, i.e., the energy per cycle multiplied by ventilating frequency, has been causally linked to VILI risk [3], not all combinations of the three pressure components of energy and frequency that sum to the same total power value are equally hazardous. For injury to occur, a second requirement (apart from the raw power total) is a precondition; enough strain per cycle must be imposed to sufficiently distort lung parenchyma or disrupt vulnerable elements of the extracellular matrix that comprise the interdependent supporting framework for the alveolar network. The strain actually experienced at the tissue level depends on local force-amplifying influences such as geometrical stress focusing and rate of parenchymal expansion [4]. Duration of exposure (which determines the cumulative number of high stress cycles) is clearly of importance once the injuring strain threshold has been breached. Finally, whether or not a given pattern of ventilation injures also depends on lung capacity and innate vulnerability of lung tissues to the applied mechanical stress. Thus, a healthy lung can withstand power loads much greater than do the relatively fragile but functional alveoli that make up the “baby lung” of ARDS [5]. Sub-components and thresholds of tidal energy Regarding the monitored variables of ventilation that relate to total inflation pressure, active debate has developed as to whether the element with most influence is endinspiratory static (plateau) pressure or its difference from PEEP, known as the driving pressure (ΔP) [6–8]. PEEP bears a U-shaped relationship to VILI risk, with low levels tending to reduce atelectasis and distribute stress [9, 10]. On the other hand, high PEEP sets an elevated platform from which widespread tidal overstretching of the parenchyma as well as hemodynamic compromise become increasingly likely [10]. Finally, neither PEEP, plateau pressure, nor their difference (ΔP) reflect the dynamics and dissipated energy of the tidal cycle. While energy clearly must be expended to produce damaging strain, uncertainty exists regarding which component of the applied energy per inflation cycle deserves closest attention. As implied by the earlier discussion, the “energy envelope” of tidal inflation encloses a total pressure-volume area defined by the combination of the flow-resistive, tidal elastic and PEEP-associated sectors that comprise it (Fig. 1a). Although flow-resistive energy largely dissipates in pushing gas past the endotracheal tube and through conducting airways, rapid movements of parenchymal tissues induce greater strains than slower ones—both during inflation and deflation [4, 11, 12]. The influence of PEEP-related inflation energy often has been discounted as well, using the reasoning that the pressure baseline is eventually recovered at the end of the deflation phase [8, 13]. Whatever the perceived wisdom of that argument, PEEP undeniably elevates volume and strain over the resting values of their fully relaxed states. In so doing, raising PEEP requires that each inflation volume increment is achieved at higher absolute pressure and with greater energy input. The driving pressure (tidal elastic) component of inflation

Which component of mechanical power is most important in causing VILI?