Effect of tracheal gas insufflation on gas exchange in canine oleic acid- induced lung injury

A. Nahum, A. Chandra, J. Niknam, S. A. Ravenscraft, A. B. Adams, J. J. Marini

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Objective: To determine the effect of tracheal gas insufflation on gas exchange in oleic acid-induced lung injury in dogs. Design: Prospective, longitudinal study. Setting: University research laboratory. Subjects: Five mongrel dogs. Interventions: The dogs were anesthetized, paralyzed, and mechanically ventilated. Lung injury was induced by infusing 0.09 mL/kg of oleic acid and pulmonary artery occlusion (wedge) pressure (PAOP) was increased to 15 mm Hg by infusing fluids to enhance pulmonary edema formation. After 60 mins, PAOP was allowed to decrease to 5 mm Hg and was maintained at 5 mm Hg for 60 mins to stabilize the pulmonary edema. We studied the effect of tracheal gas insufflation on gas exchange at low and high end-expiratory lung volumes achieved by a positive end-expiratory pressure of 5 and 12 cm H2O, respectively. The FIO2 values of the ventilator and catheter were equivalent (0.6). Each tracheal gas insufflation stage at low and high end-expiratory lung volume was preceded and followed by conventional mechanical ventilation stages without tracheal gas insufflation. During transitions between conventional mechanical ventilation and tracheal gas insufflation, end-expiratory lung volume was maintained constant by adjusting positive end-expiratory pressure while monitoring esophageal pressure and inductive plethysmography. Tidal volume was maintained constant throughout the protocol (0.40 L). Measurements and Main Results. At each stage, we measured PaCO2, PaO2, total physiologic deadspace fraction, and venous admixture, which were 43 ± 4 torr (5.7 ± 0.5 kPa), 325 ± 6 torr (43.3 ± 0.8 kPa), 53 ± 3%, and 4.0 ± 0.3% before oleic acid lung injury, respectively. After oleic acid injury at low end-expiratory lung volume, these variables were 55 ± 4 tort (7.3 ± 0.5 kPa), 73 ± 13 torr (9.7 ± 1.7 kPa), 61 ± 4%, and 50 ± 7%, respectively. During tracheal gas insufflation at low end-expiratory lung volume conditions, PaCO2 and the total physiologic deadspace fraction decreased significantly (p < .05) to 45 ± 4 torr (6.0 ± 0.5 kPa) and 50 ± 5%, respectively. Under high end-expiratory lung volume conditions, PaCO2 and the total physiologic deadspace fraction were 55 ± 7 torr (7.3 ± 0.9 kPa) and 61 ± 6%, respectively; during tracheal gas insufflation, these variables decreased to 43 ± 4 torr (5.7 ± 0.5 kPa) and 52 ± 5%, respectively (p < .05). Increasing end-expiratory lung volume improved both PaO2 and venous admixture (p < .05) but tracheal gas insufflation had no significant effect on oxygenation efficiency when end- expiratory lung volume was held constant. Conclusions: Tracheal gas insufflation augmented alveolar ventilation effectively in the setting of oleic acid-induced lung injury in dogs. When end-expiratory lung volume and tidal volume were kept constant, tracheal gas insufflation did not affect oxygenation.

Original languageEnglish (US)
Pages (from-to)348-356
Number of pages9
JournalCritical care medicine
Volume23
Issue number2
DOIs
StatePublished - Feb 21 1995

Keywords

  • cardiopulmonary emergencies
  • critical illness
  • gas exchange
  • lung injury
  • lungs
  • mechanical ventilation
  • mechanical ventilation
  • oleic acid
  • tidal volume
  • tracheal gas insufflation

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