RESPIRATORISCHE UND HAMODYNAMISCHE FOLGEN EINER EINSEITIGEN INHALATIONSVERLETZUNG DER LUNGE

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. The diversion of pulmonary blood flow from more severely damaged areas to better ventilated areas maintains the PaO₂ within the normal physiological range. In a second phase, progressive mechanical airway obstruction, release of vasoconstrictive mediators, and cellular plugging of the pulmonary vasculature result in an increase of pulmonary arterial pressure, which then leads to progressive failure of the compensatory adaptation phenomena.