Atelectrauma Versus Volutrauma: A Tale of Two Time-Constants

Abstract

Objectives: Elucidate how the degree of ventilator-induced lung injury due to atelectrauma that is produced in the injured lung during mechanical ventilation is determined by both the timing and magnitude of the airway pressure profile.

Design: A computational model of the injured lung provides a platform for exploring how mechanical ventilation parameters potentially modulate atelectrauma and volutrauma. This model incorporates the time dependence of lung recruitment and derecruitment, and the time-constant of lung emptying during expiration as determined by overall compliance and resistance of the respiratory system.

Setting: Computational model.

Subjects: Simulated scenarios representing patients with both normal and acutely injured lungs.

Measurements and main results: Protective low-tidal volume ventilation (Low-Vt) of the simulated injured lung avoided atelectrauma through the elevation of positive end-expiratory pressure while maintaining fixed tidal volume and driving pressure. In contrast, airway pressure release ventilation avoided atelectrauma by incorporating a very brief expiratory duration () that both prevents enough time for derecruitment and limits the minimum alveolar pressure prior to inspiration. Model simulations demonstrated that has an effective threshold value below which airway pressure release ventilation is safe from atelectrauma while maintaining a tidal volume and driving pressure comparable with those of Low-Vt. This threshold is strongly influenced by the time-constant of lung-emptying.

Conclusions: Low-Vt and airway pressure release ventilation represent markedly different strategies for the avoidance of ventilator-induced lung injury, primarily involving the manipulation of positive end-expiratory pressure and , respectively. can be based on exhalation flow values, which may provide a patient-specific approach to protective ventilation.

Keywords: acute respiratory distress syndrome; computational model; lung elastance; mechanical ventilation; recruitment and derecruitment; ventilator-induced lung injury; volutrauma.

Figure 1.

Model schematic and example behavior. A, Single-compartment model of the lung; the alveolar compartment expands vertically to represent tissue distension and horizontally to represent recruitment. B, Simulated profiles of airway pressure and flow during pressure-controlled low-Vt ventilation (solid lines) and airway pressure release ventilation (dashed lines).

Figure 2.

Calibration of model to experimental data. A, Respiratory system elastance versus time in mice following recruitment maneuvers given at t = 0 at three different positive end-expiratory pressure (PEEP) levels (adapted from a previous study [10] with permission from the American Physiologic Society). Open symbols: baseline conditions; closed symbols: lung injury; circles: PEEP = 1 cm H₂O; squares: PEEP = 3 cm H₂O; triangles: PEEP = 6 cm H₂O. B, Elastance profiles simulated using the model. Solid lines: baseline conditions; dashed lines: lung injury.

Figure 3.

Atelectrauma index (), driving pressure (P_driving), and tidal volume as a function of positive end-expiratory pressure (PEEP) for Low-Vt ventilation for (A) = 10 s and (B) = 2 s. Peak airway pressure was 10 cm H₂O above PEEP in all cases. Dashed lines: healthy lung; solid lines: injured lung. Note that remains relatively high until PEEP reaches approximately 15 cm H₂O.

Figure 4.

Atelectrauma index (), driving pressure (P_driving), and tidal volume as a function of for low-Vt ventilation for (A) = 10 s and (B) = 2 s. Peak airway pressure was 10 cm H₂O above positive end-expiratory pressure in all cases. Dashed lines: healthy lung; solid lines: injured lung. Note that is low until reaches approximately 0.5 s, after which it rises dramatically as is further increased.

Figure 5.

Model predictions of the atelectrauma index () as a function of during ventilation of the injured lung with airway pressure release ventilation for (A) = 10 s and (B) = 2 s, showing the effects of reducing the time-constant of emptying of the lung achieved by varying airway resistance (Raw).