Driving pressure and mechanical power: new targets for VILI prevention

Abstract

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 cmH2O/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.

Keywords: Mechanical ventilation; atelectrauma; barotrauma; driving pressure; ergotrauma; mechanical power; ventilator-induced lung injury (VILI); volutrauma.

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1

Evolution of the concept of VILI. From left to right: barotrauma (2), volutrauma (3), atelectrauma/biotrauma (4), ergotrauma (5). VILI, ventilator-induced lung injury.

Figure 2

Graphical representation of Mead’s model of lung stress (20). The highest lung stress is always concentrated around the totally collapsed units.

Figure 3

The diagram represents the time-course of experimental ventilator-induced lung injury. As shown, the first lesions appear after 10–15 h and are mainly represented by small CT opacities at the interface between the visceral and the parietal pleura. After 15 h the process becomes exponential and after 25 h the opacities involve all the lung parenchyma (34).

Figure 4

Graphical representation of the equation of power (22). The upper left rectangle (∆V × PEEP) represents the baseline stretch of the fibers, i.e., the energy level to be overcome at each tidal volume delivery. The blue triangle (1/2 × Ers × ∆V) represents the energy needed to win the elasticity of the respiratory system. The orange parallelogram (F × Raw × ∆V) represents the energy needed to win the resistance to the gas flow. The lower green triangle represents the static component of PEEP (i.e., PEEP multiplied by the PEEP volume), not taking part in the equation of power, as it is delivered just once (at the first application/change of PEEP).