Atelectasis: its evolution during upper urinary tract surgery.
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Severe intraoperative hypoxaemia occurred in a previously healthy 19-yr-old accident victim. Although rare, major lung collapse secondary to mucous plugging should be considered in the differential diagnosis of intraoperative hypoxaemia, particularly following major trauma.
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Apnoeic left lower lobes of dog lungs were inflated by increasing alveolar pressure or decreasing pleural pressure, or the lobes were collapsed and exposed to decreasing pleural pressure with the bronchus occluded. Under each of these conditions the lobe could be made 'hypoxic' by perfusion with mixed venous blood or 'normoxic' by perfusion with systemic arterial blood. Inflation of the lobes diminished the hypoxic presor response. The relative influence of decreasing pleural pressure on inflated and collapsed lobes was such that at low pleural pressures resistance to flow through the hypoxic atelectatic lobe was no greater than that through the inflated normoxic lobe. The results indicated that the level of lung inflation can alter the effectiveness of the hypoxic pressor response in reducing perfusion to underventilated regions.
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Twenty patients (23-76 yr) were studied with regard to lung tissue changes prior to and following induction of general anesthesia with muscular relaxation, and another four subjects were studied for a longer period awake. The transverse thoracic area and the structure of the lung tissue were determined by computerized tomography. No abnormalities in the lung tissue were noted before anesthesia. Within 5 min after induction, including muscular relaxation, all subjects had developed crest-shaped changes of increased density in the dependent regions of both lungs. They were largest in the most caudal segment (4.8 +/- 0.8% of the transverse lung area, mean +/- SE) and smaller in the cephalad exposures (3.4 +/- 0.7% of the transverse area). The size of the densities showed no correlation to age. The densities did not increase after a further 20 min of anesthesia and were not affected by the inspiratory oxygen fraction. When the subjects were moved from the supine to the lateral position, the crest-shaped densities disappeared in the nondependent lung and remained in the dorsal part of the dependent lung. The application of positive end-expiratory pressure of 10 cmH2O eliminated or reduced the densities. The four awake subjects showed no lung densities after 90 min in the supine position. It is suggested that these crest-shaped densities represent atelectases, which develop by compression of lung tissue rather than by resorption of gas.
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