title: Hypothermic low-flow cardiopulmonary bypass impairs pulmonary and right ventricular function more than circulatory arrest.
abstract: BACKGROUND
  Hypothermic circulatory arrest (HCA) is used during surgical treatment of certain congenital heart defects. The possibility of ischemic neurologic injury associated with HCA has led some surgeons to use low-flow cardiopulmonary bypass (CPB) during the hypothermic interval (hypothermic low flow [HLF]). This study investigates the inflammatory response to HCA and HLF, and reports the consequences of this response on pulmonary and right ventricular function.
  
  
  METHODS
  Piglets (3.1 to 6.6 kg) were cooled to 16 degrees to 18 degrees C using CPB, and randomized: HCA for 60 minutes (n = 7), or HLF (50 cc.kg(-1).min(-1)) for 60 minutes (n = 6). The piglets were rewarmed to 36 degrees C and weaned from CPB. Serum tumor necrosis factor-alpha (TNF-alpha) concentration, percent lung water, and pulmonary and cardiac function were measured before and after CPB.
  
  
  RESULTS
  Tumor necrosis factor-alpha was higher after HLF (2,990.5 +/- 884.5 pg/mL), compared with HCA (347.6 +/- 89.2 pg/mL; p = 0.03). The percent lung water was higher after HLF (84.8% +/- 0.3%) than HCA (82.0% +/- 0.4%; p < 0.001). The alveolar to arterial oxygen gradient was worse after HLF (457 +/- 42 mm Hg) than HCA (285.8 +/- 45 mm Hg; p = 0.02). Pulmonary vascular resistance was greater after HLF (36.08 +/- 8.28 mm Hg.mL(-1).m(-2).min(-1)) than HCA (14.55 +/- 3.46 mm Hg. mL(-1).m(-2).min(-1); p = 0.049). The right ventricular pressure waveform peak derivative, corrected for systolic pulmonary artery pressure, was lower after HLF (14.1 +/- 1.4 sec(-1)), than HCA (23.8 +/- 2.7 sec(-1); p = 0.01).
  
  
  CONCLUSIONS
  Hypothermic low flow extends exposure to CPB, and is associated with an increased inflammatory response compared with HCA. The greater inflammatory response after HLF may result in substantial nonneurologic morbidity in the postoperative period, demonstrated by pulmonary and right ventricular dysfunction. Interventions that attenuate the inflammatory response to CPB may prevent pulmonary and right ventricular dysfunction after HLF.
authors.affiliation: Division of Pediatric Cardiac Surgery, Doernbecher Children's Hospital, Oregon Health and Science University, Portland, Oregon 97239-3098, USA.
authors.forename: Jess M
authors.initials: JM
authors.lastname: Schultz
authors.forename: Tara
authors.initials: T
authors.lastname: Karamlou
authors.forename: Julia
authors.initials: J
authors.lastname: Swanson
authors.forename: Irving
authors.initials: I
authors.lastname: Shen
authors.forename: Ross M
authors.initials: RM
authors.lastname: Ungerleider
mesh_terms: D000818:Animals; D001794:Blood Pressure; D050792:Circulatory Arrest, Deep Hypothermia Induced / Q000009:adverse effects* / Q000379:methods*; D006324:Heart Arrest, Induced / Q000009:adverse effects* / Q000379:methods*; D006330:Heart Defects, Congenital / Q000601:surgery; D007249:Inflammation; D008168:Lung / Q000098:blood supply / Q000737:chemistry; D011897:Random Allocation; D012129:Respiratory Function Tests; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014655:Vascular Resistance; D016278:Ventricular Function, Right; D014867:Water / Q000032:analysis
chemical_list: D014409:Tumor Necrosis Factor-alpha; D014867:Water