Samenvatting

Introduction High mechanical power is associated with mortality in patients who are critically ill and require invasive ventilation. It remains uncertain which components of mechanical power – volume, pressure or rate – increase mechanical power the most. Methods We conducted a post hoc analysis of a database containing individual patient data from three randomised clinical trials of ventilation in patients without acute respiratory distress syndrome. The primary endpoint was mechanical power. We used linear regression; double stratification to create subgroups of participants; and mediation analysis to assess the impact of changes in volumes, pressures and rates on mechanical power. Results A total of 1732 patients were included and analysed. The median (IQR [range]) mechanical power was 12.3 (9.3–17.1 [3.7–50.1]) J.min-1. In linear regression, respiratory rate (36%) and peak pressure (51%) explained most of the increase in mechanical power. Increasing quintiles of peak pressure stratified on constant levels of respiratory rate resulted in higher risks of high mechanical power (relative risk 2.2 (95%CI 1.8–2.6), p < 0.01), while decreasing quintiles of respiratory rate stratified on constant levels of peak pressure resulted in lower risks of high mechanical power (relative risk 0.2 (95%CI 0.2–0.3), p < 0.01). Mediation analysis showed that a reduction in respiratory rate, with the increase in tidal volume, partially mediates an effect of reduction in mechanical power (average causal mediation effect -0.10, 95%CI -0.12 to -0.09, p < 0.01), but still with a direct effect of tidal volume on mechanical power (average direct effect 0.15, 95%CI 0.11–0.19, p < 0.01). Discussion In this cohort of patients without acute respiratory distress syndrome, pressure and respiratory rate were the most important determinants of mechanical power. The respiratory rate may be the most attractive ventilator setting to adjust when targeting a lower mechanical power.