Biologically variable ventilation increases arterial oxygenation over that seen with positive end-expiratory pressure alone in a porcine model of acute respiratory distress syndrome.
OBJECTIVE
We compared biologically variable ventilation (BVV) (as previously described) (1) with conventional control mode ventilation (CV) in a model of acute respiratory distress syndrome (ARDS) both at 10 cm H2O positive end-expiratory pressure.


METHODS
Randomized, controlled, prospective study.


METHODS
University research laboratory.


METHODS
Farm-raised 3- to 4-month-old swine.


METHODS
Oleic acid (OA) was infused at 0.2 mL/kg/hr with FIO2 = 0.5 and 5 cm H2O positive end-expiratory pressure until PaO2 was < or =60 mm Hg; then all animals were placed on an additional 5 cm H2O positive end-expiratory pressure for the next 4 hrs. Animals were assigned randomly to continue CV (n = 9) or to have CV computer controlled to deliver BVV (variable respiratory rate and tidal volume; n = 8). Hemodynamic, expired gas, airway pressure, and volume data were obtained at baseline (before OA), immediately after OA, and then at 60-min intervals for 4 hrs.


RESULTS
At 4 hrs after OA injury, significantly higher PaO2 (213+/-17 vs. 123+/-47 mm Hg; mean+/-SD), lower shunt fraction (6%+/-1% vs. 18%+/-14%), and lower PaCO2 (50+/-8 vs. 65+/-11 mm Hg) were seen with BVV than with CV. Respiratory system compliance was greater by experiment completion with BVV (0.37+/-0.05 vs. 0.31+/-0.08 mL/cm H2O/kg). The improvements in oxygenation, CO2 elimination, and respiratory mechanics occurred without a significant increase in either mean airway pressure (14.3+/-0.9 vs. 14.9+/-1.1 cm H2O) or mean peak airway pressure (39.3+/-3.5 vs. 44.5+/-7.2 cm H2O) with BVV. The oxygen index increased five-fold with OA injury and decreased to significantly lower levels over time with BVV.


CONCLUSIONS
In this model of ARDS, BVV with 10 cm H2O positive end-expiratory pressure improved arterial oxygenation over and above that seen with CV with positive end-expiratory pressure alone. Proposed mechanisms for BVV efficacy are discussed.
Department of Anesthesia and Neuroanesthesia Research Laboratory, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
W A
WA
Mutch
S
S
Harms
G R
GR
Lefevre
M R
MR
Graham
L G
LG
Girling
S E
SE
Kowalski
D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004195:Disease Models, Animal; D004298:Dopamine / Q000627:therapeutic use; D006439:Hemodynamics / Q000187:drug effects; D019301:Oleic Acid; D010100:Oxygen / Q000097:blood*; D011175:Positive-Pressure Respiration; D011659:Pulmonary Gas Exchange; D012121:Respiration, Artificial / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000139:chemically induced / Q000628:therapy*; D013552:Swine; D013990:Tidal Volume / Q000187:drug effects
D002316:Cardiotonic Agents; D019301:Oleic Acid; D010100:Oxygen; D004298:Dopamine