Abstract
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.
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.
| Original language | English |
|---|---|
| Pages (from-to) | 533-542 |
| Journal | Anaesthesia |
| Volume | 80 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2025 |
Funding
The three original studies used for the analysis were registered at ClinicalTrials.gov (NCT02159196, NCT02153294 and NCT03167580) and all trials were supported in full by peer-reviewed grants from ZonMW, Netherlands Organization for Health Research and Development and endorsed by the Academic Medical Centre (Amsterdam, the Netherlands). For this current analysis, no additional funding was received.
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