title: [Respiratory and hemodynamic sequelae of unilateral inhalation injury of the lung].
abstract: Respiratory failure after smoke inhalation injury is usually preceded by a 12-48 h interval with only minor clinical symptoms. Since pulmonary lesions show a patchy distribution, it has been postulated that vasoconstriction in more severely damaged areas induces a shift of pulmonary blood flow to less severely damaged areas, minimizing venous admixture. This hypothesis was tested in a sheep model in which only one lung was exposed to smoke. Six chronically instrumented (arterial, central venous, pulmonary artery thermodilution, and left atrial catheters; ultrasonic transit time flow probe around the left pulmonary artery) range ewes were intubated with a modified Carlens tube under halothane anesthesia. Smoke from smoldering cotton was insufflated into the left lung until a carboxyhemoglobin level of 50% was achieved. After the smoking procedure, the animals were awakened, extubated, and studied for 24 h. During this time, the pulmonary vascular resistance of the left lungs increased fourfold while the pulmonary vascular resistance of both lungs only doubled. Left pulmonary artery blood flow decreased progressively to 37% of control at 24 h, while cardiac output decreased by only 25%. PaO2 decreased from 107 +/- 12 to 77 +/- 15 mmHg at 24 h. Mean pulmonary arterial pressure rose from 18 to 23 mmHg. Heart rate, mean arterial pressure, left atrial pressure, and PaCO2 showed no statistically significant changes. The results indicate that the response of the pulmonary vasculature to smoke inhalation injury is a two-phase phenomenon. In the first phase, vasoconstriction occurs to counterbalance injury-induced ventilation-perfusion mismatching.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Anesthesia Research Laboratory, University of Texas Medical Branch Galveston.
authors.forename: J L
authors.initials: JL
authors.lastname: Theissen
authors.forename: T
authors.initials: T
authors.lastname: Prien
authors.forename: J
authors.initials: J
authors.lastname: Maguire
authors.forename: H L
authors.initials: HL
authors.lastname: Lübbesmeyer
authors.forename: L D
authors.initials: LD
authors.lastname: Traber
authors.forename: D N
authors.initials: DN
authors.lastname: Herndon
authors.forename: D L
authors.initials: DL
authors.lastname: Traber
mesh_terms: D000818:Animals; D001980:Bronchi / Q000473:pathology; D002059:Burns, Inhalation / Q000473:pathology / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D006439:Hemodynamics; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D011650:Pulmonary Alveoli / Q000503:physiopathology; D011659:Pulmonary Gas Exchange; D011669:Pulmonary Wedge Pressure; D012128:Respiratory Distress Syndrome / Q000503:physiopathology; D012131:Respiratory Insufficiency / Q000503:physiopathology; D012756:Sheep; D014692:Ventilation-Perfusion Ratio
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen
vernacular_title: Respiratorische und hämodynamische Folgen einer einseitigen Inhalationsverletzung der Lunge.