title: Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury.
abstract: Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. 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 with PEEPe. In seven New Zealand White 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 a fraction of inspired O(2) (Fi(O(2))) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH(2)O, and either 1) high RR (24) and low PEEPe (3.5) or 2) low RR (7) and high PEEPe (14). We assessed cyclical lung recruitment with a fast arterial Po(2) 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 with 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.
authors.affiliation: Department of Clinical Studies, Section of Critical Care, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Rebecca S
authors.initials: RS
authors.lastname: Syring
authors.forename: Cynthia M
authors.initials: CM
authors.lastname: Otto
authors.forename: Rebecca E
authors.initials: RE
authors.lastname: Spivack
authors.forename: Klaus
authors.initials: K
authors.lastname: Markstaller
authors.forename: James E
authors.initials: JE
authors.lastname: Baumgardner
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D018893:Bronchoalveolar Lavage / Q000009:adverse effects*; D002302:Cardiac Output / Q000502:physiology; D004195:Disease Models, Animal; D045853:Exhalation / Q000502:physiology*; D005260:Female; D008168:Lung / Q000503:physiopathology; D055370:Lung Injury; D008448:Maximal Expiratory Flow Rate / Q000502:physiology; D011175:Positive-Pressure Respiration / Q000379:methods*; D001261:Pulmonary Atelectasis / Q000209:etiology* / Q000503:physiopathology*; D011817:Rabbits; D015656:Respiratory Mechanics / Q000502:physiology; D012965:Sodium Chloride
chemical_list: D012965:Sodium Chloride