Effects of Similar Mechanical Power Resulting From Different Combinations of Respiratory Variables on Lung Damage in Experimental Acute Respiratory Distress Syndrome.

Summary

In an LPS-induced rat ARDS model ventilated for 80 minutes at equal mechanical power, very-high tidal volume/very-low respiratory rate caused greater histologic injury and biomarker derangements than low tidal volume/high rate. Plateau and driving pressures rose with increasing tidal volume, indicating that mechanical power alone does not capture VILI risk—how its components are delivered matters.

Key Findings

• At equal mechanical power, very-high Vt/very-low RR produced greater overdistension, edema, and injury markers than low Vt/high RR.
• Inflammatory (IL-6), stretch (amphiregulin), epithelial (SP-B), endothelial (VCAM-1, Ang-2), and ECM (versican, syndecan) biomarkers were highest with very-high Vt.
• Plateau and driving pressures increased stepwise from low to high Vt settings.

Clinical Implications

Clinicians should avoid high tidal volumes and driving pressures even if mechanical power targets are met; power metrics should be contextualized with plateau/driving pressures and tissue strain indicators.

Limitations

• Short ventilation duration (80 minutes) limits applicability to clinical time scales
• Findings from rodent models may not fully translate to human ARDS physiology

Future Directions

Test power-component interactions in large-animal models and incorporate power plus driving/plateau constraints in ventilator protocols and clinical trials.