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1 Department of Clinical Studies, Section of Critical Care, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
2 Department of Anesthesiology, Johannes Gutenberg University, Mainz, Germany; Department of Anesthesiology and Critical Care, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
3 Department of Anesthesiology and Critical Care, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States; Oscillogy LLC, Folsom, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: baumgarj{at}uphs.upenn.edu.
Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic PEEP (PEEPe) can maintain alveolar recruitment at end-exhalation, but PEEPe depresses cardiac output and increases overdistention. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared to PEEPe. In seven NZW rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with FIO2 of 1.0, I:E of 2:1, and Pplat of 28 cmH2O, and either: (a) high RR (24) and low PEEPe (3.5); or (b) low RR (7) and high PEEPe (14). We assessed cyclical lung recruitment with a fast arterial PO2 probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared to the high PEEPe group (p < 0.001) and mixed venous saturation was consistently greater in the high RR group (p < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.
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J. E. Baumgardner and R. S. Syring Reply to Costa and Amato J Appl Physiol, June 1, 2007; 102(6): 2415 - 2415. [Full Text] [PDF]
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