Atelectasis and surfactant depletion may contribute to greater distension—and thereby injury—of aerated lung regions; recruitment of atelectatic lung may protect these regions by attenuating such overdistension. However, the effects of atelectasis (and recruitment) on aerated airspaces remain elusive. We tested the hypothesis that during mechanical ventilation, surfactant depletion increases the dimensions of aerated airspaces and that lung recruitment reverses these changes.
Prospective imaging study in an animal model.
Research imaging facility.
Twenty-seven healthy Sprague Dawley rats.
Surfactant depletion was obtained by saline lavage in anesthetized, ventilated rats. Alveolar recruitment was accomplished using positive end-expiratory pressure and exogenous surfactant administration.
Airspace dimensions were estimated by measuring the apparent diffusion coefficient of 3He, using diffusion-weighted hyperpolarized gas magnetic resonance imaging. Atelectasis was demonstrated using computerized tomography and by measuring oxygenation. Saline lavage increased atelectasis (increase in nonaerated tissue from 1.2% to 13.8% of imaged area, p < 0.001), and produced a concomitant increase in mean apparent diffusion coefficient (~33%, p < 0.001) vs. baseline; the heterogeneity of the computerized tomography signal and the variance of apparent diffusion coefficient were also increased. Application of positive end-expiratory pressure and surfactant reduced the mean apparent diffusion coefficient (~23%, p < 0.001), and its variance, in parallel to alveolar recruitment (i.e., less computerized tomography densities and heterogeneity, increased oxygenation).
Overdistension of aerated lung occurs during atelectasis is detectable using clinically relevant magnetic resonance imaging technology, and could be a key factor in the generation of lung injury during mechanical ventilation. Lung recruitment by higher positive end-expiratory pressure and surfactant administration reduces airspace distension.
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1 Department of Anesthesiology and Critical Care and Stavropoulos Sepsis Research Program, University of Pennsylvania, Philadelphia, PA.
2 Department of Radiology, University of Pennsylvania, Philadelphia, PA.
3 Department of Otolaryngology–Head & Neck Surgery, Johns Hopkins University, Baltimore, MD.
4 Departments of Critical Care Medicine and Anesthesia, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
*See also p. 683.
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Dr. Emami is currently affiliated with Polarean, Durham, NC.Other than Dr. Kavanagh, all other authors have received funding from the National Institutes of Health. The remaining authors have not disclosed any potential conflicts of interest.
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