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Effect of Positive End-Expiratory Pressure on Regional Lung Expansion of Oleic Acid-Injured Dogs* FREE TO VIEW

M. A. Martynowicz, MD; T. A. Minor, MD; T. A. Wilson, MD; B. J. Walters; R. D. Hubmayr, MD, FCCP
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*From the Mayo Clinic, Rochester, MN.

Correspondence to: Marek Martynowicz, MD, Pulmonary and Critical Care, Mayo Clinic, 200 First St SW, Rochester, MD 55905

Chest. 1999;116(suppl_1):28S-29S. doi:10.1378/chest.116.suppl_1.28S
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In previous studies on oleic acid (OA)-injured dogs, we have shown that dependent lung need not be compressed or atelectatic; it is airless but expanded by edema (Am J Respir Crit Care Med 1997; 155:A859). This observation challenges the idea that positive end-expiratory pressure (PEEP) recruits units simply by opposing the deforming stress produced by the weight of the edematous lungs. To characterize the effects of PEEP on lung recruitment in OA-injured dogs, we measured in situ spirograms of five caudal lobes during sinusoidal oscillations above airway pressures of 0, 7.5, and 15 cm H2O. Each lobe contained 10 to 15 previously implanted metallic markers, the displacements of which were recorded using biplane fluoroscopy and tracked using an operator-interactive image analysis system. Each marker formed the apex of a polyhedron containing air, blood, tissue, and edema fluid; its volume defined the in situ expansion of the region. Each region’s functional residual capacity (FRCr) and oscillation amplitude (VTr) was computed and normalized by its preinjury volume at total lung capacity. In prone dogs, the region of interest was nondependent and presumably aerated. In supine animals, it was dependent and presumably flooded. In prone animals, OA produced an average FRCr reduction of 14%, whereas VTr increased by 18%. With animals in the supine posture, OA produced a 5% increase in FRCr, whereas VTr declined to 25% of baseline. Injury responses were identical at the oscillation rates of 2.5 and 20 cycles per minute. In prone animals, PEEP of 7.5 and 15 cm H2O raised FRCr of the nondependent lobe by an average of 37% and 108%, respectively, whereas VTr declined with progressive hyperinflation. In supine animals, the effect of PEEP on FRCr was less pronounced, more variable, and at times uncoupled from the VTr responses. In some instances, PEEP reestablished lobar tidal oscillations with only small increases in FRCr, whereas in others, FRCr rose without substantial changes in VTr. A consistent observation across all animals, postures, and oscillation frequencies was a PEEP-induced shift of the dynamic regional transpulmonary pressure-volume curves to higher volumes. This suggests that even large distending pressures when applied intermittently during individual breaths are ineffective in producing full recruitment. We conclude that the temporal and topographic heterogeneity of an injured lung’s response to PEEP cannot be adequately explained by a simple model with a gravitational volume gradient and that mechanisms involved in the translocation of edema fluid from airways and alveolar spaces must be considered.

Supported by NIH HL-57364.




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