Fatigue-aware alveolar stress and strain tracking: a theoretical biomechanics framework for regional mechanical dose accumulation in ventilator-induced lung injury

Ventilator-induced lung injury remains incompletely explained by global bedside variables that do not resolve regional load, deformation, time, repetition, and recovery. FAAST (Fatigue-Aware Alveolar Stress and Strain Tracking) and its deterministic implementation, FAAST2, describe regional mechanical exposure and fatigue. The framework maps a shared central-airway boundary into 20 compartments, defines functional-residual-capacity-referenced volumetric strain, closes generalized constitutive stress through regional specific elastance, and tracks Time-Accumulated Stress History (TASH), the complete-cycle load-time channel, and Strain-Accumulated Strain History (SASH), the cumulative positive loading-branch deformation-work channel. A cycle-indexed Continuum of Damage Index (CDI) combines elemental load-time and deformation-work increments with inherited fatigue. CDI is irreversible and bounded; a continuous recovery-opportunity factor accelerates decay of reversible fatigue memory rather than subtracting accumulated damage. Applying selected ventilation values from Park’s ALS report with declared PEEP and normal-lung mechanics produced a chronic-stability comparator with 1-h Strain-Accumulated Strain History 88.9 kPa, dynamic strain 0.194, per-cycle deformation work 0.098 kPa, recovery opportunity 0.827, and bounded steady fatigue 0.015; CDI was not extrapolated across chronic support. Relative to this comparator, 1-h regional SASH across Cases 1–4H was 99.5, 485.1, 723.8, and 1,510.4 kPa, or 1.12, 5.46, 8.14, and 17.0 times the comparator, respectively; illustrative 24-h maximum compartment CDI was 0.280, 0.478, 0.618, and 0.851. Higher tidal volume increased burden despite fewer breaths, while a preferentially loaded compliant region in heterogeneous ARDS carried the greatest burden. A matched OSCILLATE sensitivity applied reported day-1 arm settings to the same Panwar-H-anchored 20-compartment lung for 24 h. In the compartment attaining maximum CDI at 24 h, control ventilation produced Time-Accumulated Stress History 28.080 kPa·h, SASH 15,496 kPa, and maximum compartment CDI 0.596. Across declared HFOV tracheal oscillatory tidal-volume sensitivities of 0.5–2.0 mL/kg predicted body weight, TASH was approximately 31.299 kPa·h, SASH ranged from 13,513 to 54,053 kPa, and CDI ranged from 0.575 to 0.777. Modeled SASH arm equivalence occurred at 0.573 mL/kg; this is a mechanical comparison point, not an injury threshold. These are ecological sensitivity outputs, not measured HFOV tidal volumes, patient reconstructions, time-weighted exposures, mortality predictions, or evidence that pulmonary mechanics exclude hemodynamic harm. FAAST2 requires regional construct validation and biological calibration before clinical use.

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Publication Details

Journal
Frontiers in Bioengineering and Biotechnology
Published
2026-11-09
DOI
https://doi.org/10.3389/fbioe.2026.1938944
Primary Topic
Respiratory Support and Mechanisms
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article
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article

Fatigue-aware alveolar stress and strain tracking: a theoretical biomechanics framework for regional mechanical dose accumulation in ventilator-induced lung injury

Michael Champagne
Frontiers in Bioengineering and Biotechnology
Respiratory Support and Mechanisms
article

Fatigue-aware alveolar stress and strain tracking: a theoretical biomechanics framework for regional mechanical dose accumulation in ventilator-induced lung injury

Michael Champagne
article en

Abstract

Ventilator-induced lung injury remains incompletely explained by global bedside variables that do not resolve regional load, deformation, time, repetition, and recovery. FAAST (Fatigue-Aware Alveolar Stress and Strain Tracking) and its deterministic implementation, FAAST2, describe regional mechanical exposure and fatigue. The framework maps a shared central-airway boundary into 20 compartments, defines functional-residual-capacity-referenced volumetric strain, closes generalized constitutive stress through regional specific elastance, and tracks Time-Accumulated Stress History (TASH), the complete-cycle load-time channel, and Strain-Accumulated Strain History (SASH), the cumulative positive loading-branch deformation-work channel. A cycle-indexed Continuum of Damage Index (CDI) combines elemental load-time and deformation-work increments with inherited fatigue. CDI is irreversible and bounded; a continuous recovery-opportunity factor accelerates decay of reversible fatigue memory rather than subtracting accumulated damage. Applying selected ventilation values from Park’s ALS report with declared PEEP and normal-lung mechanics produced a chronic-stability comparator with 1-h Strain-Accumulated Strain History 88.9 kPa, dynamic strain 0.194, per-cycle deformation work 0.098 kPa, recovery opportunity 0.827, and bounded steady fatigue 0.015; CDI was not extrapolated across chronic support. Relative to this comparator, 1-h regional SASH across Cases 1–4H was 99.5, 485.1, 723.8, and 1,510.4 kPa, or 1.12, 5.46, 8.14, and 17.0 times the comparator, respectively; illustrative 24-h maximum compartment CDI was 0.280, 0.478, 0.618, and 0.851. Higher tidal volume increased burden despite fewer breaths, while a preferentially loaded compliant region in heterogeneous ARDS carried the greatest burden. A matched OSCILLATE sensitivity applied reported day-1 arm settings to the same Panwar-H-anchored 20-compartment lung for 24 h. In the compartment attaining maximum CDI at 24 h, control ventilation produced Time-Accumulated Stress History 28.080 kPa·h, SASH 15,496 kPa, and maximum compartment CDI 0.596. Across declared HFOV tracheal oscillatory tidal-volume sensitivities of 0.5–2.0 mL/kg predicted body weight, TASH was approximately 31.299 kPa·h, SASH ranged from 13,513 to 54,053 kPa, and CDI ranged from 0.575 to 0.777. Modeled SASH arm equivalence occurred at 0.573 mL/kg; this is a mechanical comparison point, not an injury threshold. These are ecological sensitivity outputs, not measured HFOV tidal volumes, patient reconstructions, time-weighted exposures, mortality predictions, or evidence that pulmonary mechanics exclude hemodynamic harm. FAAST2 requires regional construct validation and biological calibration before clinical use.

Frontiers in Bioengineering and BiotechnologyVol. 14
Respiratory Support and Mechanisms
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