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Effects of Respiratory Rate, Plateau Pressure, and Positive End-Expiratory Pressure on Pa_O2 Oscillations after Saline Lavage

Departments of Anesthesia, Clinical Studies-Philadelphia, School of Veterinary Medicine, and Center for Sleep and Respiratory Neurobiology, University of Pennsylvania, Philadelphia; SpectruMedix LLC, State College, Pennsylvania; Departments of Anesthesiology and Radiology, Johannes Gutenberg-University, Mainz; and Department of Anesthesiology and Intensive Care Medicine, Ernst-Moritz-Arndt-University, Greifswald, Germany

Correspondence and requests for reprints should be addressed to James E. Baumgardner, M.D., Ph.D., Department of Anesthesia, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104-4283. E-mail: baumgarj{at}uphs.upenn.edu

One of the proposed mechanisms of ventilator-associated lung injury is cyclic recruitment of atelectasis. Collapse of dependent lung regions with every breath should lead to large oscillations in Pa_O2 as shunt varies throughout the respiratory cycle. We placed a fluorescence-quenching PO₂ probe in the brachiocephalic artery of six anesthetized rabbits after saline lavage. Using pressure-controlled ventilation with oxygen, ventilator settings were varied in random order over three levels of positive end-expiratory pressure (PEEP), respiratory rate (RR), and plateau pressure minus PEEP (). Dependence of the amplitude of Pa_O2 oscillations on PEEP, RR, and was modeled by multiple linear regression. Before lavage, arterial PO₂ oscillations varied from 3 to 22 mm Hg. After lavage, arterial PO₂ oscillations varied from 5 to 439 mm Hg. Response surfaces showed markedly nonlinear dependence of amplitude on PEEP, RR, and . The large Pa_O2 oscillations observed provide evidence for cyclic recruitment in this model of lung injury. The important effect of RR on the magnitude of Pa_O2 oscillations suggests that the static behavior of atelectasis cannot be accurately extrapolated to predict dynamic behavior at realistic breathing frequencies.

Key Words: respiratory distress syndrome • atelectasis • cyclic recruitment • ventilator-associated lung injury

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