title: Matching positive end-expiratory pressure to intra-abdominal pressure prevents end-expiratory lung volume decline in a pig model of intra-abdominal hypertension.
abstract: OBJECTIVE
  Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. In a previous experimental study, positive end-expiratory pressures of up to 15 cm H2O did not prevent end-expiratory lung volume decline caused by intra-abdominal hypertension. Therefore, we examined the effect of matching positive end-expiratory pressure to the intra-abdominal pressure on cardio-respiratory parameters.
  
  
  METHODS
  Experimental pig model of intra-abdominal hypertension.
  
  
  METHODS
  Large animal facility, University of Western Australia.
  
  
  METHODS
  Nine anesthetized, nonparalyzed, and ventilated pigs (48 ± 7 kg).
  
  
  METHODS
  Four levels of intra-abdominal pressure (baseline, 12, 18, and 22 mm Hg) were generated in a randomized order by inflating an intra-abdominal balloon. At each level of intra-abdominal pressure, three levels of positive end-expiratory pressure were randomly applied with varying degrees of matching the corresponding intra-abdominal pressure: baseline positive end-expiratory pressure (= 5 cm H2O), moderate positive end-expiratory pressure (= half intra-abdominal pressure in cm H2O + 5 cm H2O), and high positive end-expiratory pressure (= intra-abdominal pressure in cm H2O).
  
  
  METHODS
  We measured end-expiratory lung volume, arterial oxygen levels, respiratory mechanics, and cardiac output 5 mins after each new intra-abdominal pressure and positive end-expiratory pressure setting.
  
  
  RESULTS
  Intra-abdominal hypertension decreased end-expiratory lung volume and PaO2 (-49% [p < .001] and -8% [p < .05], respectively, at 22 mm Hg intra-abdominal pressure compared with baseline intra-abdominal pressure) but did not change cardiac output (p = .5). At each level of intra-abdominal pressure, moderate positive end-expiratory pressure increased end-expiratory lung volume (+119% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) while minimally decreasing cardiac output (-8%, p < .05). High positive end-expiratory pressure further increased end-expiratory lung volume (+233% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) but led to a greater decrease in cardiac output (-26%, p < .05). Neither moderate nor high positive end-expiratory pressure improved PaO2 (p = .7). Intra-abdominal hypertension decreased end-expiratory transpulmonary pressure but did not alter end-inspiratory transpulmonary pressure. Intra-abdominal hypertension decreased total respiratory compliance through a decrease in chest wall compliance. Positive end-expiratory pressure decreased the respiratory compliance by reducing lung compliance.
  
  
  CONCLUSIONS
  In a pig model of intra-abdominal hypertension, positive end-expiratory pressure matched to intra-abdominal pressure led to a preservation of end-expiratory lung volume, but did not improve arterial oxygen tension and caused a reduction in cardiac output. Therefore, we do not recommend routine application of positive end-expiratory pressure matched to intra-abdominal pressure to prevent intra-abdominal pressure-induced end-expiratory lung volume decline in healthy lungs.
authors.affiliation: Intensive Care Unit, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia. adrian.regli@gmail.com
authors.forename: Adrian
authors.initials: A
authors.lastname: Regli
authors.forename: Jakob
authors.initials: J
authors.lastname: Chakera
authors.forename: Bart L
authors.initials: BL
authors.lastname: De Keulenaer
authors.forename: Brigit
authors.initials: B
authors.lastname: Roberts
authors.forename: Bill
authors.initials: B
authors.lastname: Noffsinger
authors.forename: Bhajan
authors.initials: B
authors.lastname: Singh
authors.forename: Peter V
authors.initials: PV
authors.lastname: van Heerden
mesh_terms: D034841:Abdominal Cavity / Q000503:physiopathology*; D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D004195:Disease Models, Animal; D059325:Intra-Abdominal Hypertension / Q000503:physiopathology*; D008176:Lung Volume Measurements; D008297:Male; D010100:Oxygen / Q000097:blood; D011175:Positive-Pressure Respiration / Q000379:methods*; D011312:Pressure; D011897:Random Allocation; D034421:Sus scrofa; D013990:Tidal Volume / Q000502:physiology
chemical_list: D010100:Oxygen