Airway closure, atelectasis and gas exchange during general anaesthesia.

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.

Volumetric analysis of aeration in the lungs during general anaesthesia.

Spiral computed tomography (CT) allows volumetric analysis of formation of atelectasis and aeration of the lungs during anaesthesia. We studied 26 premedicated patients undergoing elective surgery allocated to group 1 (conscious, spontaneous breathing, investigating inspiration and expiration), group 2 (general anaesthesia with mechanical ventilation, investigating inspiration and expiration) or group 3 (general anaesthesia with mechanical ventilation, investigating changes over time). Using spiral CT, the lungs were studied either before or during general anaesthesia. CT scans were grouped into the following areas: overaeration, normal aeration, reduced aeration, poor aeration and atelectasis. The mechanism of atelectasis appeared to be both gravitational forces and a diaphragm-related force that acts regionally in caudal lung regions. Mean atelectasis formation and poorly aerated regions comprised approximately 4% of the total lung volume between the diaphragm and carina, giving a mean value of 16-20% of the normal aerated lung tissue being either collapsed or poorly aerated. The vertical ventilation distribution was more even during anaesthesia than in the awake state.

Atelectasis and pulmonary shunting during induction of general anaesthesia--can they be avoided?

BACKGROUND: Gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. A major cause of this disorder appears to be atelectasis and consequently pulmonary shunt. After re-expansion, atelectasis reappears very slowly if 30% oxygen in nitrogen is used, but much faster if 100% oxygen is used. The aim of the present study-was to evaluate if early formation of atelectasis and pulmonary shunt may be avoided if the lungs are ventilated with 30% oxygen in nitrogen instead of 100% oxygen during the induction of general anaesthesia. METHODS: Twenty-four adult patients with healthy lungs scheduled for elective surgery were investigated. During induction of anaesthesia, the lungs were manually ventilated via a face mask, using either 30% oxygen in nitrogen (group 1, n = 12) or 100% oxygen (group 2, n = 12). Atelectasis was estimated by computed x-ray tomography and ventilation-perfusion distribution with the multiple inert gas elimination technique, both awake and during general anaesthesia with mechanical ventilation. RESULTS: No atelectasis was present in the awake subjects. After induction of anaesthesia, the mean amount of atelectasis was minor (0.2 +/- 0.4 cm2) in group 1 and considerably greater (8.0 +/- 8.2 cm2) in group 2 (P < 0.001). The pulmonary shunt was 0.3 +/- 0.7% of cardiac output in the awake subjects. This value increased to 2.1 +/- 3.8% in group 1 and to 6.5 +/- 5.2% in group 2 (P < 0.05). The indices of VA/Q mismatch showed no difference between the two groups. CONCLUSION: During induction of general intravenous anaesthesia in patients with healthy lungs, gas composition plays an important role for atelectasis formation and the establishment of pulmonary shunt. By using a mixture containing 30% oxygen in nitrogen, the early formation of atelectasis and pulmonary shunt may, at least in part, be avoided.

Prevention of atelectasis during general anaesthesia.

Atelectasis is an important cause of impaired gas exchange during general anaesthesia; it causes pulmonary shunting. We studied the effects of gas composition on the formation of atelectasis and on gas exchange during the induction of general anaesthesia. In 12 adult patients, the lungs were ventilated with 30% oxygen in nitrogen during anaesthesia induction, and in another 12, a conventional technique was used (100% oxygen during induction and 40% oxygen in nitrogen thereafter). Extent of atelectasis was estimated by computed tomography and the ventilation-perfusion relation (VA/Q) by the multiple inert gas elimination technique. After anaesthesia induction, there was little atelectasis in the 30% oxygen group (mean 0.2 [SD 0.4] cm2) and a significantly greater amount (4.2 [5-6] cm2; p < 0.001) in the 100% oxygen group. Patients in the 30% oxygen group were observed for another 40 min. 6 continued to receive 30% oxygen (subgroup A) and 6 were ventilated with 100% oxygen (subgroup B). During this time, the amount of atelectasis increased to 1.6 (1.6) cm2 in subgroup A and to 4.7 (4.5) cm2 in subgroup B (p = 0.047 for difference between groups). In subgroup A, the shunt (VA/Q < 0.005) increased from 1.6 (2.0)% of cardiac output to 3.2 (2.7)%, but the arterial oxygen tension did not change. In subgroup B, the shunt increased from 2.6 (5.2)% to 9.8 (5.7)% of cardiac output. These results suggest that the composition of inspired gas is important in atelectasis formation during general anaesthesia. Use of a lower oxygen concentration than is now standard practice might prevent the early formation of atelectasis.

Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia.

BACKGROUND: Atelectasis, an important cause of impaired gas exchange during general anesthesia, may be eliminated by a vital capacity maneuver. However, it is not clear whether such a maneuver will have a sustained effect. The aim of this study was to determine the impact of gas composition on reappearance of atelectasis and impairment of gas exchange after a vital capacity maneuver. METHODS: A consecutive sample of 12 adults with healthy lungs who were scheduled for elective surgery were studied. Thirty minutes after induction of anesthesia with fentanyl and propofol, the lungs were hyperinflated manually up to an airway pressure of 40 cmH2O. FIO2 was either kept at 0.4 (group 1, n = 6) or changed to 1.0 (group 2, n = 6) during the recruitment maneuver. Atelectasis was assessed by computed tomography. The amount of dense areas was measured at end-expiration in a transverse plane at the base of the lungs. The ventilation-perfusion distributions (VA/Q) were estimated with the multiple inert gas elimination technique. The static compliance of the total respiratory system (Crs) was measured with the flow interruption technique. RESULTS: In group 1 (FIO2 = 0.4), the recruitment maneuver virtually eliminated atelectasis for at least 40 min, reduced shunt (VA/Q < 0.005), and increased at the same time the relative perfusion to poorly ventilated lung units (0.005 < VA/Q < 0.1; mean values are given). The arterial oxygen tension (PaO2) increased from 137 mmHg (18.3 kPa) to 163 mmHg (21.7 kPa; before and 40 min after recruitment, respectively; P = 0.028). In contrast to these findings, atelectasis recurred within 5 min after recruitment in group 2 (FIO2 = 1.0). Comparing the values before and 40 min after recruitment, all parameters of VA/Q were unchanged. In both groups, Crs increased from 57.1/55.0 ml.cmH2O-1 (group 1/group 2) before to 70.1/67.4 ml.cmH2O-1 after the recruitment maneuver. Crs showed a slow decrease thereafter (40 min after recruitment: 61.4/60.0 ml.cmH2O-1), with no difference between the two groups. CONCLUSIONS: 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.

Reexpansion of atelectasis during general anaesthesia may have a prolonged effect.

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.

Re-expansion of atelectasis during general anaesthesia: a computed tomography study.

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.