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; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. Results In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r2 = 0.41, P = 0.001) and lung elastance (r2 = 0.33, P < 0.01) and decrease in Pao2/Fio2 (r2 = 0.40, P < 0.001) at the end of the study. Conclusion In piglets, VILI develops if a mechanical power threshold is exceeded.

Clinicaltrials.gov identifier: NCT01670747 ( www.clinicaltrials.gov ).

Background: Mechanical power (MP) is the energy delivered to the respiratory system over time during mechanical ventilation. Our aim was to compare the currently available methods to calculate MP during volumeand pressure-controlled ventilation, comparing different equations with the geometric reference method, to understand whether the easier to use surrogate formulas were suitable for the everyday clinical practice. This would warrant a more widespread use of mechanical power to promote lung protection. Methods: Forty respiratory failure patients, sedated and paralyzed for clinical reasons, were ventilated in volumecontrolled ventilation, at two inspiratory flows (30 and 60 L/min), and pressure-controlled ventilation with a similar tidal volume. Mechanical power was computed both with the geometric method, as the area between the inspiratory limb of the airway pressure and the volume, and with two algebraic methods, a comprehensive and a surrogate formula. Results: The bias between the MP computed by the geometric method and by the comprehensive algebraic method during volume-controlled ventilation was respectively 0.053 (0.77, − 0.81) J/min and − 0.4 (0.70, − 1.50) J/ min at low and high flows (r 2 = 0.96 and 0.97, p < 0.01). The MP measured and computed by the two methods were highly correlated (r 2 = 0.95 and 0.94, p < 0.01) with a bias of − 0.0074 (0.91, − 0.93) and − 1.0 (0.45, − 2.52) J/ min at high-low flows. During pressure-controlled ventilation, the bias between the MP measured and the one calculated with the comprehensive and simplified methods was correlated (r 2 = 0.81, 0.94, p < 0.01) with mean differences of − 0.001 (2.05, − 2.05) and − 0.81 (2.11, − 0.48) J/min. Conclusions: Both for volume-controlled and pressure-controlled ventilation, the surrogate formulas approximate the reference method well enough to warrant their use in the everyday clinical practice. Given that these formulas require nothing more than the variables already displayed by the intensive care ventilator, a more widespread use of mechanical power should be encouraged to promote lung protection against ventilator-induced lung injury.

Background: Bedside measures of patient effort are essential to properly titrate the level of pressure support ventilation. We investigated whether the tidal swing in oesophageal (DPes) and transdiaphragmatic pressure (DPdi), and ultrasonographic changes in diaphragm (TFdi) and parasternal intercostal (TFic) thickening are reliable estimates of respiratory effort. The effect of diaphragm dysfunction was also considered. Methods: Twenty-one critically ill patients were enrolled: age 73 ( 14) yr, BMI 27 (7) kg m À2 , and PaO 2 /FIO 2 33.3 (9.2) kPa. A three-level pressure support trial was performed: baseline, 25% (PS-medium), and 50% reduction (PS-low). We recorded the oesophageal and transdiaphragmatic pressureetime products (PTPs), work of breathing (WOB), and diaphragm and intercostal ultrasonography. Diaphragm dysfunction was defined by the Gilbert index.Results: Pressure support was 9.0 (1.6) cm H 2 O at baseline, 6.7 (1.3) (PS-medium), and 4.4 (1.0) (PS-low). DPes was significantly associated with the oesophageal PTP (R 2 ¼0.868; P<0.001) and the WOB (R 2 ¼0.683; P<0.001). DPdi was significantly associated with the transdiaphragmatic PTP (R 2 ¼0.820; P<0.001). TFdi was only weakly correlated with the oesophageal PTP (R 2 ¼0.326; P<0.001), and the correlation improved after excluding patients with diaphragm dysfunction (R 2 ¼0.887; P<0.001). TFdi was higher and TFic lower in patients without diaphragm dysfunction: 33.6 (18.2)% vs 13.2 (9.2)% and 2.1 (1.7)% vs 12.7 (9.1)%; P<0.0001.Conclusions: DPes and DPdi are adequate estimates of inspiratory effort. Diaphragm ultrasonography is a reliable indicator of inspiratory effort in the absence of diaphragm dysfunction. Additional measurement of parasternal intercostal thickening may discriminate a low inspiratory effort or a high effort in the presence of a dysfunctional diaphragm.