An estimation of mechanical stress on alveolar walls during repetitive alveolar reopening and closure

Abstract

Alveolar overdistension and mechanical stresses generated by repetitive opening and closing of small airways and alveoli have been widely recognized as two primary mechanistic factors that may contribute to the development of ventilator-induced lung injury. A long-duration exposure of alveolar epithelial cells to even small, shear stresses could lead to the changes in cytoskeleton and the production of inflammatory mediators. In this paper, we have made an attempt to estimate in situ the magnitudes of mechanical stresses exerted on the alveolar walls during repetitive alveolar reopening by using a tape-peeling model of McEwan and Taylor (35). To this end, we first speculate the possible ranges of capillary number (Ca) ≡ μU/γ (a dimensionless combination of surface tension γ, fluid viscosity μ, and alveolar opening velocity U) during in vivo alveolar opening. Subsequent calculations show that increasing respiratory rate or inflation rate serves to increase the values of mechanical stresses. For a normal lung, the predicted maximum shear stresses are <15 dyn/cm(2) at all respiratory rates, whereas for a lung with elevated surface tension or viscosity, the maximum shear stress will notably increase, even at a slow respiratory rate. Similarly, the increased pressure gradients in the case of elevated surface or viscosity may lead to a pressure drop >300 dyn/cm(2) across a cell, possibly inducing epithelial hydraulic cracks. In addition, we have conceived of a geometrical model of alveolar opening to make a prediction of the positive end-expiratory pressure (PEEP) required to splint open a collapsed alveolus, which as shown by our results, covers a wide range of pressures, from several centimeters to dozens of centimeters of water, strongly depending on the underlying pulmonary conditions. The establishment of adequate regional ventilation-to-perfusion ratios may prevent recruited alveoli from reabsorption atelectasis and accordingly, reduce the required levels of PEEP. The present study and several recent animal experiments likewise suggest that a lung-protective ventilation strategy should not only include small tidal volume and plateau pressure limitations but also consider such cofactors as ventilation frequency and inflation rate.

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“…Moreover, dynamic stress and strain, both undisputed contributors to VILI [17,18,19,20], are reduced in FCV due to steady, slow changes in pressure and smooth increase or decrease in lung volume during the whole ventilation cycle at an optimally low RR (see digital content: Additional le 1).…”

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“…This may induce alveolar overdistention or mechanical shear stress on airways and alveolar epithelial cells, with the potential for cell and tissue damage. 17 We have considered MI-E because it was the device available for our subjects. They were adapted to use it and not other devices.…”

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“…3, A and B, and Supplemental Animation S3). This leads to a large dynamic alveolar strain, which is known to be a primary VILI mechanism (1,17). Pathologic changes in alveolar stability can be identified using a deep inflation (DI) and measuring the change in elastance (H) and hysteresivity ().…”