title: Tracheal gas insufflation improves ventilatory efficiency during metacholine-induced bronchospasm.
abstract: BACKGROUND
  Barotrauma and cardiovascular insufficiency are frequently encountered problems in patients with acute bronchospastic disease who require mechanical ventilation. Permissive hypercapnia is a recognized strategy for minimizing these adverse effects; however, it has potential risks. Tracheal gas insufflation (TGI) has been shown to increase carbon dioxide elimination efficiency and thus could permit mechanical ventilation at lower peak airway pressures without inducing hypercapnia. However, caution exists as to the impact of TGI on lung volumes, given that expiratory flow limitation is a hallmark of bronchospastic disease.
  
  
  OBJECTIVE
  To examine these issues, we studied ventilatory and hemodynamic effects of continuous TGI as an adjunct to mechanical ventilation before and after methacholine-induced bronchospasm.
  
  
  METHODS
  Ten anesthetized, paralyzed dogs were ventilated on volume-controlled mechanical ventilation during administration of continuous TGI (0, 2, 6, and 10 L/min) while total inspired minute ventilation (ventilator-derived minute ventilation plus TGI) was kept constant. In an additional step, with TGI flow of 10 L/min, total inspired minute ventilation was decreased by 30%.
  
  
  RESULTS
  PaCO2 decreased (44 +/- 7 mm Hg at zero flow to 34 +/- 7 mm Hg at 6 L/min and 31 +/- 6 mm Hg at 10 L/min, respectively, P < .05), as did the dead space to tidal volume ratio at TGI of 6 and 10 L/min compared with zero flow. There were no significant changes in end-expiratory transpulmonary pressure, mean arterial pressure, or cardiac output. During the highest TGI flow (10 L/min), with a 30% reduction of total inspired minute ventilation, both PaCO2 and peak airway pressure remained less than during zero flow conditions.
  
  
  CONCLUSIONS
  We conclude that TGI increases carbon dioxide elimination efficiency during constant and decreased minute ventilation conditions without any evidence of hyperinflation or hemodynamic instability during methacholine-induced bronchospasm.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, School of Medicine, Pittsburgh, PA 15261, USA.
authors.forename: A M
authors.initials: AM
authors.lastname: Miro
authors.forename: L A
authors.initials: LA
authors.lastname: Hoffman
authors.forename: F J
authors.initials: FJ
authors.lastname: Tasota
authors.forename: D W
authors.initials: DW
authors.lastname: Sigler
authors.forename: D T
authors.initials: DT
authors.lastname: Gowski
authors.forename: J
authors.initials: J
authors.lastname: Lutz
authors.forename: T
authors.initials: T
authors.lastname: Zullo
authors.forename: M R
authors.initials: MR
authors.lastname: Pinsky
mesh_terms: D000818:Animals; D001986:Bronchial Spasm / Q000139:chemically induced / Q000628:therapy*; D016085:Bronchoconstrictor Agents; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D006439:Hemodynamics; D007327:Insufflation / Q000379:methods*; D016210:Methacholine Chloride; D010102:Oxygen Inhalation Therapy / Q000379:methods*; D011659:Pulmonary Gas Exchange; D012121:Respiration, Artificial; D014132:Trachea
chemical_list: D016085:Bronchoconstrictor Agents; D016210:Methacholine Chloride