Energy dissipation during mechanical ventilation: Alveolar recruitment is the likely cause of VILI.

Introduction::
Introduction: Acute respiratory distress syndrome (ARDS) is a prevalent and often fatal medical condition that is typically treated through supportive mechanical ventilation. Unfortunately, this intervention frequently results in ventilator-induced lung injury (VILI). Despite the development of low-tidal volume ventilation as a protective approach for ARDS, mortality rates remain alarmingly high at 30-40%. Recent research has examined the potential role of energy delivery and dissipation in the respiratory system as a contributing factor to VILI. Therefore, the present investigation was conducted to assess and analyze energy delivery and dissipation mechanisms through carefully controlled experiments carried out in a porcine model of ARDS.




Materials and Methods::
Methods: All experiments were conducted with approval from the SUNY Upstate Medical University Institutional Animal Care and Use Committee in accordance with ARRIVE guidelines. To simulate the pathophysiology of ARDS, a 3% Tween-20 detergent solution (0.75 mL/kg) was precisely instilled into only dependent basilar lung regions. The animals were anesthetized and then paralyzed with rocuronium and ventilated with an airway pressure release ventilation (APRV) mode to control overdistension (OD) and recruitment/derecruitment (RD) independently: OD+ was produced by establishing a P_High = 40 cmH₂O; OD- was induced by applying a PHigh = 28 cmH₂O; RD+ was produced by prolonging T_Low to allow the lung units to collapse, and RD- was induced by utilizing a brief T_Low to hinder derecruitment during exhalation. Each treatment (OD+RD+, OD-RD+, OD+RD-, OD-RD-) was studied with a 10-pig cohort.









We measured the PaO2/FiO2 ratio over a 6-hour period during experiments with and without OD and RD to quantify physiological recovery over a 6-hour timeframe. Energy delivery and dissipation information were obtained from Pressure-Volume (PV) loops where we classified the individual dissipation contributions from 1) airflow, 2) tissue/surfactant, and 3) recruitment as shown schematically in Figure 1.




Results, Conclusions, and Discussions::
Results: We found that neither total energy delivery nor total energy dissipation demonstrated a correlation with physiological recovery. Only the recruitment component of dissipated energy showed a correlation with physiological recovery, as shown in Fig. 2, and accounted for only ~3% of the total energy dissipation. We also estimated the energy dissipation associated with recruitment of a single alveolus to be ~10nJ. This energy is delivered over a very brief time interval, however, giving a power flux (power/area) of approximately 100W/m², which is approximately 10% of the intensity of the sun at the earth’s surface.









Conclusions: Our study demonstrates that when the amount of power dissipated to the lungs through recruitment is below a certain threshold, recovery from lavage injury occurs quickly. Conversely, there was no recovery observed if 5-10% of alveoli undergo repetitive recruitment/derecruitment. These findings strongly suggest that recruitment energy dissipation is the primary cause of VILI, which leads to the conclusion that minimizing recruitment and derecruitment is critical to mitigating the risk of VILI.




Acknowledgements (Optional): : This work was supported by NIH grant R01HL142702

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