Formation of atelectasis is one mechanism of impaired gas exchange during general anaesthesia. We have studied manoeuvres to re-expand such atelectasis in 16 consecutive, anaesthetized adults with healthy lungs. In group 1 (10 patients), the lungs were inflated stepwise to an airway pressure (Paw) of 10, 20, 30 and 40 cm H2O. In group 2 (six patients), three repeated inflations up to Paw = 30 cm H2O were followed by one inflation to 40 cm H2O. Atelectasis was assessed by analysis of computed x-ray tomography (CT). In group 1 the mean area of atelectasis in the CT scan at the level of the right diaphragm was 6.4 cm2 at Paw = 0 cm H2O, 5.9 cm2 at 20 cm H2O, 3.5 cm2 at 30 cm H2O and 0.8 cm2 at 40 cm H2O. A Paw of 20 cm H2O corresponds approximately to inflation with twice the tidal volume. In group 2 the mean area of atelectasis was 9.0 cm2 at Paw = 0 cm H2O and 4.2 cm2 after the first inflation to 30 cm H2O. Repeated inflations did not add to re-expansion of atelectasis. The final inflation (Paw = 40 cm H2O) virtually eliminated the atelectasis. We conclude that, after induction of anaesthesia, the amount of atelectasis was not reduced by inflation of the lungs with a conventional tidal volume or with a double tidal volume ("sigg"). An inflation to vital capacity (Paw = 40 cm H2O), however, re-expanded virtually all atelectatic lung tissue.

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The composition of inspiratory gas plays an important role in the recurrence of collapse of previously reexpanded atelectatic lung tissue during general anesthesia in patients with healthy lungs. The reason for the instability of these lung units remains to be established. The change in the amount of atelectasis and shunt appears to be independent of the change in the compliance of the respiratory system.

Airway closure and the formation of atelectasis have been proposed as important contributors to impairment of gas exchange during general anaesthesia. We have elucidated the relationships between each of these two mechanisms and gas exchange. We studied 35 adults with healthy lungs, undergoing elective surgery. Airway closure was measured using the foreign gas bolus technique, atelectasis was estimated by analysis of computed x-ray tomography, and ventilation-perfusion distribution (VA/Q) was assessed by the multiple inert gas elimination technique. The difference between closing volume and expiratory reserve volume (CV-ERV) increased from the awake to the anaesthetized state. Linear correlations were found between atelectasis and shunt (r = 0.68, P < 0.001), and between CV-ERV and the amount of perfusion to poorly ventilated lung units ("low Va/Q", r = 0.57, P = 0.001). Taken together, the amount of atelectasis and airway closure may explain 75% of the deterioration in PaO2. There was no significant correlation between CV-ERV and atelectasis. We conclude that in anaesthetized adults with healthy lungs, undergoing mechanical ventilation, both airway closure and atelectasis contributed to impairment of gas exchange. Atelectasis and airway closure do not seem to be closely related.

Pulmonary atelectasis, as found during general anaesthesia, may be reexpanded by hyper-inflation of the lungs. The purpose of this study was to determine whether such a recruitment is maintained and whether this is accompanied by an improved gas exchange. We studied a consecutive sample of twelve lung healthy adults, scheduled for elective surgery. After induction of intravenous anaesthesia, the lungs were hyperinflated manually. The ventilationperfusion relationship (VA/Q) was estimated with the multiple inert gas method, and in six patients atelectasis was assessed by computed x-ray tomography. The mean pulmonary shunt was 7.5% of cardiac output after induction of anaesthesia and this decreased to 1.0% and 2.8% at 20 and 40 min after the recruitment manoeuvre. Perfusion of poorly ventilated lung regions (low VA/Q), however, increased from 3.7% to 10.6% and 7.8% at 20 and 40 min after the recruitment, respectively. The mean alveolar-arterial oxygen tension difference (PA-aO2) was 14.3 kPa after induction of anaesthesia and 11.1 kPa immediately after recruitment. Forty minutes later PA-aO2 was still 2.0 kPa lower than after induction of anaesthesia (95% confidence interval [CI] 0.3 to 3.8 kPa). PA-aO2 decreased more in obese patients. The mean area of atelectasis decreased from 9.0 cm2 after induction of anaesthesia to 0.1 cm2 immediately after recruitment, and there was a slow increase to 1.9 cm2 (95% CI 0.0 to 3.9 cm2) 40 min later. During general anaesthesia in lung healthy patients, most of the reexpanded atelectatic lung tissue remains inflated for at least 40 min. The recruitment manoeuvre decreases pulmonary shunt, but increases low VA/Q. The net effect on gas exchange is a small reduction of PA-aO2.