Neurally adjusted ventilatory assist decreases  ventilator-induced lung injury  and non-pulmonary organ dysfunction  in rabbits with acute lung injury.
OBJECTIVE
To determine if neurally adjusted ventilatory assist (NAVA) that delivers pressure in proportion to diaphragm electrical activity is as protective to acutely injured lungs (ALI) and non-pulmonary organs as volume controlled (VC), low tidal volume (Vt), high positive end-expiratory pressure (PEEP) ventilation.


METHODS
Prospective, randomized, laboratory animal study.


METHODS
Twenty-seven male New Zealand white rabbits.


METHODS
Anesthetized rabbits with hydrochloric acid-induced ALI were randomized (n = 9 per group) to 5.5 h NAVA (non-paralyzed), VC (paralyzed; Vt 6-ml/kg), or VC (paralyzed; Vt 15-ml/kg). PEEP was adjusted to hemodynamic goals in NAVA and VC6-ml/kg, and was 1 cmH2O in VC15-ml/kg.


RESULTS
PaO2/FiO2; lung wet-to-dry ratio; lung histology; interleukin-8 (IL-8) concentrations in broncho-alveolar-lavage (BAL) fluid, plasma, and non-pulmonary organs; plasminogen activator inhibitor type-1 and tissue factor in BAL fluid and plasma; non-pulmonary organ apoptosis rate; creatinine clearance; echocardiography. PEEP was similar in NAVA and VC6-ml/kg. During NAVA, Vt was lower (3.1 +/- 0.9 ml/kg), whereas PaO2/ FiO2, respiratory rate, and PaCO2 were higher compared to VC6-ml/kg (p<0.05 for all). Variables assessing ventilator-induced lung injury (VILI), IL-8 levels, non-pulmonary organ apoptosis rate, and kidney as well as cardiac performance were similar in NAVA compared to VC6-ml/kg. VILI and non-pulmonary organ dysfunction was attenuated in both groups compared to VC15-ml/kg.


CONCLUSIONS
In anesthetized rabbits with early experimental ALI, NAVA is as effective as VC6-ml/kg in preventing VILI, in attenuating excessive systemic and remote organ inflammation, and in preserving cardiac and kidney function.
Brander
Lukas
L
Interdepartmental Division of Critical Care Medicine, Department of Critical Care Medicine, University of Toronto, St. Michael's Hospital, Toronto, ON M5B 1W8, Canada.
Sinderby
Christer
C
Lecomte
François
F
Leong-Poi
Howard
H
Bell
David
D
Beck
Jennifer
J
Tsoporis
James N
JN
Vaschetto
Rosanna
R
Schultz
Marcus J
MJ
Parker
Thomas G
TG
Villar
Jesús
J
Zhang
Haibo
H
Slutsky
Arthur S
AS
D055371:Acute Lung Injury / Q000503:physiopathology / Q000628:therapy*; D000704:Analysis of Variance; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D003964:Diaphragm / Q000503:physiopathology; D004195:Disease Models, Animal; D055724:Electrophysiological Phenomena / Q000502:physiology; D025461:Feedback, Physiological / Q000502:physiology*; D016209:Interleukin-8 / Q000032:analysis / Q000097:blood; D008297:Male; D009102:Multiple Organ Failure / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis / Q000097:blood; D011175:Positive-Pressure Respiration / Q000009:adverse effects / Q000379:methods; D011446:Prospective Studies; D011817:Rabbits; D011897:Random Allocation; D012121:Respiration, Artificial / Q000009:adverse effects / Q000379:methods*; D018709:Statistics, Nonparametric; D013925:Thromboplastin / Q000032:analysis; D013990:Tidal Volume / Q000502:physiology*; D055397:Ventilator-Induced Lung Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*
D016209:Interleukin-8; D017395:Plasminogen Activator Inhibitor 1; D013925:Thromboplastin