title: Tidal lung recruitment and exhaled nitric oxide during coronary artery bypass grafting in patients with and without chronic obstructive pulmonary disease.
abstract: BACKGROUND
  We studied the occurrence of intraoperative tidal alveolar recruitment/derecruitment, exhaled nitric oxide (eNO), and lung dysfunction in patients with and without chronic obstructive pulmonary disease (COPD) undergoing coronary artery bypass grafting (CABG).
  
  
  METHODS
  We performed a prospective observational physiological study at a university hospital. Respiratory mechanics, shunt, and eNO were assessed in moderate COPD patients undergoing on-pump (n = 12) and off-pump (n = 8) CABG and on-pump controls (n = 8) before sternotomy (baseline), after sternotomy and before cardiopulmonary bypass (CPB), and following CPB before and after chest closure. Respiratory system resistance (R                            (rs)), elastance (E                            (rs)), and stress index (to quantify tidal recruitment) were estimated using regression analysis. eNO was measured with chemiluminescence.
  
  
  RESULTS
  Mechanical evidence of tidal recruitment/derecruitment (stress index <1.0) was observed in all patients, with stress index <0.8 in 29% of measurements. Rrs in on-pump COPD was larger than in controls (p < 0.05). Ers increased in controls from baseline to end of surgery (19.4 ± 5.5 to 27.0 ± 8.5 ml cm H(2)O(-1), p < 0.01), associated with increased shunt (p < 0.05). Neither Ers nor shunt increased significantly in the COPD on-pump group. eNO was comparable in the control (11.7 ± 7.0 ppb) and COPD on-pump (9.9 ± 6.8 ppb) groups at baseline, and decreased similarly by 29% at end of surgery(p < 0.05). Changes in eNO were not correlated to changes in lung function.
  
  
  CONCLUSIONS
  Tidal recruitment/derecruitment occurs frequently during CABG and represents a risk for ventilator-associated lung injury. eNO changes are consistent with small airway injury, including that from tidal recruitment injury. However, those changes are not correlated with respiratory dysfunction. Controls have higher susceptibility to develop complete lung derecruitment.
authors.affiliation: Laboratory of Respiration Physiology, Carlos Chagas Filho Institute of Biophysics, Rio de Janeiro, Brazil.
authors.forename: Alysson R
authors.initials: AR
authors.lastname: Carvalho
authors.forename: Fumito
authors.initials: F
authors.lastname: Ichinose
authors.forename: Ivany A
authors.initials: IA
authors.lastname: Schettino
authors.forename: Dean
authors.initials: D
authors.lastname: Hess
authors.forename: Javier
authors.initials: J
authors.lastname: Rojas
authors.forename: Antonio
authors.initials: A
authors.lastname: Giannella-Neto
authors.forename: Arvind
authors.initials: A
authors.lastname: Agnihotri
authors.forename: Jennifer
authors.initials: J
authors.lastname: Walker
authors.forename: Thomas E
authors.initials: TE
authors.lastname: MacGillivray
authors.forename: Marcos F
authors.initials: MF
authors.lastname: Vidal Melo
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001944:Breath Tests; D016022:Case-Control Studies; D001026:Coronary Artery Bypass; D045853:Exhalation / Q000502:physiology*; D005260:Female; D006331:Heart Diseases / Q000601:surgery; D006801:Humans; D008168:Lung / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012044:Regression Analysis; D015656:Respiratory Mechanics / Q000502:physiology*; D012189:Retrospective Studies; D013312:Stress, Physiological / Q000502:physiology; D013990:Tidal Volume / Q000502:physiology
chemical_list: D009569:Nitric Oxide