Biologic Impact of Mechanical Power at High and Low Tidal Volumes in Experimental Mild Acute Respiratory Distress Syndrome

Abstract

Background The authors hypothesized that low tidal volume (VT) would minimize ventilator-induced lung injury regardless of the degree of mechanical power. The authors investigated the impact of power, obtained by different combinations of VT and respiratory rate (RR), on ventilator-induced lung injury in experimental mild acute respiratory distress syndrome (ARDS). Methods Forty Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, 32 rats were randomly assigned to be mechanically ventilated (2 h) with a combination of different VT (6 ml/kg and 11 ml/kg) and RR that resulted in low and high power. Power was calculated as energy (ΔP,L2/E,L) × RR (ΔP,L = transpulmonary driving pressure; E,L = lung elastance), and was threefold higher in high than in low power groups. Eight rats were not mechanically ventilated and used for molecular biology analysis. Results Diffuse alveolar damage score, which represents the severity of edema, atelectasis, and overdistension, was increased in high VT compared to low VT, in both low (low VT: 11 [9 to 14], high VT: 18 [15 to 20]) and high (low VT: 19 [16 to 25], high VT: 29 [27 to 30]) power groups. At high VT, interleukin-6 and amphiregulin expressions were higher in high-power than in low-power groups. At high power, amphiregulin and club cell protein 16 expressions were higher in high VT than in low VT. Mechanical energy and power correlated well with diffuse alveolar damage score and interleukin-6, amphiregulin, and club cell protein 16 expression. Conclusions In experimental mild ARDS, even at low VT, high mechanical power promoted ventilator-induced lung injury. To minimize ventilator-induced lung injury, low VT should be combined with low power.

Energy transmission in mechanically ventilated children: a translational study

“…Recurrent delivery of tidal energy inflicts VILI when stress and strain exceed the limits of tissue tolerance. Experimental work linked mechanical power > 12 J/min to the development of VILI [18][19][20][21] and adverse outcome in clinical studies in adults [7,8,22]. To date, there are no pediatric studies that have examined such relationship.…”

The Association Between Mechanical Power and Mortality in Ventilated Patients with Pneumonia

“…In our study, driving pressure was not an independent factor associated with 28-day mortality in ventilated patients with severe pneumonia, but MP was an independent factor. In experimental mild ARDS of rats, even at low V T , high MP promoted VILI [27]. In a computational study, MP showed a strong correlation with the relative risk of death across all ranges of driving pressures and PEEP [28].…”

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

“…While input of cumulative total energy and total power have been experimentally demonstrated to be linked to VILI [3,14,15], exactly which delivered component or subcomponent of power best correlates with damage has not been clearly identified. For example, it might be argued that only energy that relates to driving pressure or total elastic pressure (the product of volume and absolute alveolar pressure, ΔP + PEEP) would best track stretch and VILI risk.…”

“…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.…”