Share this article on:

Prevention of Atelectasis Formation During Induction of General Anesthesia

Rusca, Marco MD*; Proietti, Stefania MD; Schnyder, Pierre MD; Frascarolo, Philippe PhD*; Hedenstierna, Göran MD, PhD; Spahn, Donat R. MD*; Magnusson, Lennart MD, PhD*

doi: 10.1213/01.ANE.0000087042.02266.F6

General anesthesia promotes atelectasis formation, which is augmented by administration of large oxygen concentrations. We studied the efficacy of positive end-expiratory pressure (PEEP) application during the induction of general anesthesia (fraction of inspired oxygen [Fio2] 1.0) to prevent atelectasis. Sixteen adult patients were randomly assigned to one of two groups. Both groups breathed 100% O2 for 5 min and, after a general anesthesia induction, mechanical ventilation via a face mask with a Fio2 of 1.0 for another 5 min before endotracheal intubation. Patients in the first group (PEEP group) had continuous positive airway pressure (CPAP) (6 cm H2O) and mechanical ventilation via a face mask with a PEEP of 6 cm H2O. No CPAP or PEEP was applied in the control group. Atelectasis, determined by computed radiograph tomography, and analysis of blood gases were measured twice: before the beginning of anesthesia and directly after the intubation. There was no difference between groups before the anesthesia induction. After endotracheal intubation, patients in the control group showed an increase of the mean area of atelectasis from 0.8% ± 0.9% to 4.1% ± 2.0% (P = 0.0002), whereas the patients of the PEEP group showed no change (0.5% ± 0.6% versus 0.4% ± 0.7%). After the intubation with a Fio2 of 1.0, Pao2 was significantly higher in the PEEP group than in the control (591 ± 54 mm Hg versus 457 ± 99 mm Hg; P = 0.005). Atelectasis formation is prevented by application of PEEP during the anesthesia induction despite the use of large oxygen concentrations, resulting in improved oxygenation.

IMPLICATIONS: Application of positive end-expiratory pressure during the induction of general anesthesia prevents atelectasis formation. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. Therefore, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management during the anesthesia induction.

Departments of *Anesthesiology and

†Diagnostic Radiology, University Hospital, Lausanne, Switzerland; and

‡Department of Clinical Physiology, University Hospital, Uppsala, Sweden

Accepted for publication July 3, 2003.

Address correspondence and reprint requests to Lennart Magnusson, MD, PhD, Department of Anesthesiology, Centre Hospitalier, Universitaire Vaudois, Chuv BH-10, CH-1011 Lausanne, Switzerland. Address e-mail to

General anesthesia, even in the lung-healthy subject, causes an increase in intrapulmonary shunt (1), which may impair oxygenation (2). The magnitude of shunt is correlated with the formation of pulmonary atelectasis (3–5). Atelectasis appears within minutes after the induction of anesthesia (6) in 85%–90% of all patients (7). The amount of atelectasis is larger in obese patients (8) or when a high fraction of inspired oxygen (Fio2) is used (9,10). Using lower Fio2 during preoxygenation prevents atelectasis formation during the induction of general anesthesia (10). This technique, however, is not recommended because it reduces the margin of safety when a potentially long period of apnea may occur because of difficulties in airway management. However, applying positive end-expiratory pressure (PEEP) after a recruitment maneuver prevents recurrence of atelectasis despite the use of 100% O2 (4), whereas atelectasis recurs within 5 min when no PEEP is applied (11). Therefore, we hypothesized that application of PEEP throughout the induction period may prevent atelectasis formation despite the use of a large concentration of O2. Prevention of atelectasis during the induction period before tracheal intubation might increase the margin of safety in case of difficult airway management.

Back to Top | Article Outline


After institutional ethics committee approval and written informed consent 16 adults, ASA status I and II, aged 16–50 yr old, with a body mass index (BMI) <27, scheduled for elective surgery were included in this prospective, randomized single-blinded study. Patients were excluded if they were hospitalized more than 24 h before operation or if they had a history or clinical signs of heart or lung disease. The estimation of the sample size was based on previous studies (4). This size was calculated to detect a difference of 50% in atelectasis between the groups, with a P = 0.05 and a power of 80%.

Patients arrived non-premedicated to the computed tomography (CT) scan. They were randomly allocated to one of two groups (Fig. 1). Both groups were administered with 100% oxygen via a face mask for 5 min. After breathing O2, anesthesia was induced with fentanyl (2 μg/kg) and propofol (2 mg/kg) followed by a continuous infusion of propofol (4–8 mg · kg−1 · h−1). To facilitate orotracheal intubation, vecuronium (0.1 mg/kg) was given. Thereafter, the lungs were mechanically ventilated via the face mask for another 5 min with 100% O2 before intubation. In the PEEP group, a face mask was applied with a positive pressure of 6 cm H2O continuous positive airway pressure (CPAP) during spontaneous ventilation and PEEP (6 cm H2O) during mechanical ventilation. In the control group, no CPAP or PEEP was applied.

Figure 1

Figure 1

A particular device was used for CPAP application (CF800, Dräger Medical, Inc, Telford, PA), and patients of the control group breathed spontaneously through this device but without positive pressure. Mechanical ventilation consisted in a tidal volume of 10 mL/kg at 10 breaths/min (Oxylog 2000, Dräger Medical). The PEEP was monitored continuously by pressure monitor system (Endotest for low pressure cuffs, Rüsch, Kernen, Germany) measured directly at the face mask.

The primary outcome was atelectasis measured with CT scanning (7,8) at two different times: first, before the induction of general anesthesia and second, 1 min after orotracheal intubation (8). A frontal scout view was made before each CT scan, and three sections of 5 mm at 120 kV and 150 mAs were obtained at end-expiratory position 1 cm above the top of the right diaphragm with a lung algorithm (GE LightSpeed, General Electric, Milwaukee, WI). The CT data were transferred on a GE Advantage Window Station. The entire left and right lungs of each scan were chosen as the region of interest by drawing the external boundaries of the lungs at the inside of the ribs and the internal boundaries along the mediastinal organs. A window setting of −1000 to +100 Hounsfield Unit (HU) was selected to assess the total lung area. Densities, considered to reflect atelectasis, were identified in dependent lung regions and delineated manually. A threshold of −100 to +100 HU was set to measure the surface of atelectatic lung area. The right and left lungs surface of atelectasis were summed and reported to the total lung surface. Only one investigator (S.P.) performed these measurements, and she was blinded to the randomization.

The secondary outcome was analysis of arterial blood gases. Samples were obtained through radial artery puncture: one before the induction of anesthesia (on room air) and one directly after the second CT scan (100% O2) (3 min after intubation). Both samples were stored on ice before measurements, which were performed immediately after the second sample was taken. Blood-gas measurements were performed using a standard technique (Rapid Lab 865, Bayer Diagnostic, Tarrytown, NY). The blood gas analyzer is automatically calibrated every hour, and according to our hospital protocol, a manual calibration is performed every morning.

Values are expressed as mean ± sd. Baseline results and atelectatic surface were compared by analysis of variance for continuous variables and with the χ2 for discrete variables. Comparison between groups for oxygenation was performed with a two-way analysis of variance for repeated one-way measurements (time). Bonferroni correction was used for multiple comparisons. P value < 0.05 was considered significant.

Back to Top | Article Outline


The two groups were similar regarding demographic characteristics (Table 1) except for BMI, which was slightly larger in control patients. CT scans before the anesthesia induction showed essentially no atelectasis (minor densities of <1% of the total lung area, and that may have included small vessels) in either group (Fig. 2). The mean atelectasis area was 0.5% ± 0.6% in the PEEP group and 0.8% ± 0.9% in control patients.

Table 1

Table 1

Figure 2

Figure 2

Directly after tracheal intubation, the amount of atelectasis significantly increased in the control group (4.1% ± 2.0%; P = 0.005) but remained unchanged in the PEEP group (0.4% ± 0.7%; P = 0.0002 compared with control) (Fig. 2 and 3).

Figure 3

Figure 3

Blood gas analysis showed no differences before the anesthesia induction (Table 2). After the anesthesia induction and intubation, while mechanical ventilation was performed with 100% oxygen, Pao2 was significantly higher and Paco2 significantly lower in the PEEP group (Table 2).

Table 2

Table 2

Back to Top | Article Outline


The major finding of the present study is that, despite the use of 100% oxygen, application of PEEP throughout the induction period effectively prevents atelectasis formation and improves oxygenation.

Another technique for the prevention of atelectasis has been previously investigated (10). This method, consisting of an administration of only 30% oxygen, was also effective in preventing atelectasis formation during the anesthesia induction. However, this technique has not been introduced in clinical practice because of concerns of an increased risk of hypoxia during anesthesia induction. Indeed, the aim of breathing O2 is to increase the margin of safety before apnea; however, the use of only 30% of oxygen may actually decrease this margin of safety. Another study shows that the administration of 80% oxygen avoids atelectasis formation, but the apnea time until hypoxemia develops is still shorter than when the administration is performed with 100% oxygen (411 seconds versus 303 seconds) (12). Conversely, preventing atelectasis formation with the application of PEEP despite the use of 100% oxygen is more likely to maintain this margin of safety; it might even increase this margin by an increase in functional residual capacity and thus in the intrapulmonary oxygen store, as shown by the higher Pao2 seen in the PEEP group (Table 2).

Atelectasis has been evaluated by CT scanning, as previously described (7). To avoid excessive radiation exposure, we chose to scan only one segment, located 1 cm above the diaphragm. This level may not be representative of the whole lung, but it seemed to be a compromise between the most affected bases of the lungs and the less affected apical regions (4).

We have not exactly measured the time taken for intubation and the delay between the end of mechanical ventilation and second CT scan. Nevertheless, no patient had a difficult intubation, and only one attempt was required in all cases. Therefore, the time between the end of mechanical ventilation and the second CT scan might not have exceeded two minutes in any case.

Impact of atelectasis on gas exchange was directly evaluated by blood gas analysis. Previous studies have shown that anesthesia induced an increase in pulmonary shunt (measured by the inert gas technique) and that the magnitude of this shunt correlated with the amount of atelectasis (3,5). Moreover, these studies have also shown a good correlation between oxygenation (Pao2) and the amount of atelectasis. Hypoxemia may occur during the induction of general anesthesia because of difficulties in airway management. Therefore, before the induction of general anesthesia, all patients are administered 100% of oxygen to increase the margin of safety (the time before hypoxemia may develop). We have shown that with the application of PEEP during the induction period, this margin is preserved while atelectasis is prevented. Moreover, PEEP increases lung volume and therefore the oxygen store, and oxygenation is improved. Therefore, the margin of safety may also be increased.

A potential risk of mechanical ventilation by mask with PEEP is exposing a sedated, paralyzed patient to stomach insufflations and, as a result, increasing the risk of regurgitation and bronchoaspiration. This risk exists with an insufflation pressure more than 20 mm Hg, which can be obtained with manual ventilation (13,14). Alarm limits of the ventilator can be set to 20 mm Hg, and it is also possible to ventilate a patient in the pressure-controlled mode, which will prevent the use of higher pressure via the face mask.

In this study, BMI differed significantly between both groups (Table 1). Control patients had a slightly larger BMI than PEEP patients but still <27 kg/m2. In one study, a weak correlation has been shown between obesity and atelectatic surface (R 2 = 0.12; P < 0.05) when 38 patients, including morbidly obese patients, were studied (15). But we have shown that for patients with a BMI <27 kg/m2, there was no correlation between BMI and atelectatic surface (16). Therefore, the small difference between the BMI of the two groups (24 versus 22 kg/m2) is unlikely to be the main cause of the difference in the atelectasis and oxygenation seen after the anesthesia induction.

There was also a significant difference regarding Paco2 after the induction between both groups. The ventilation was standardized (10 mL/kg at 10 breaths/min); therefore, the mode of ventilation could not have been the cause of this difference. This difference may have been caused by the fact that PEEP helped to maintain airways open and may therefore have increased the alveolar minute ventilation. Application of PEEP may have deleterious effects on dead space, i.e., PEEP can induce overdistension of already expanded alveoli with reduction of perfusion and therefore increase alveolar dead space. In healthy lungs, this effect is not seen until PEEP levels exceed 10–15 cm H2O (17). Nevertheless, if this phenomenon had occurred in our study, the Pao2 should have increased in the PEEP group and not decreased; therefore, application of PEEP had probably no effect on dead space in our study.

Application of CPAP (6 cm H2O) for 5 min in conscious patients followed by 5 min of mechanical ventilation with PEEP (6 cm H2O) in sedated patients is safe, simple, and well accepted by patients. This technique prevents atelectasis formation during an anesthesia induction. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. On the contrary, when the induction of general anesthesia is performed without PEEP or CPAP, mild atelectasis will develop within minutes. Increasing the margin of safety may reduce the incidence of hypoxemia episodes during general anesthesia.

Indeed, mild to moderate hypoxemia, defined as an arterial saturation of between 85% and 90%, occurs in approximately half of all patients undergoing elective surgery, and the hypoxemia can last from a few seconds to up to 30 minutes (2). More alarming is the fact that approximately 20% of the patients may suffer from severe hypoxemia, i.e., the oxygen saturation is less than 81% for up to 5 min during anesthesia (2). Thirty-three percent of hypoxemic events occur during anesthesia induction, one-third during surgery and the last third during awakening and in the postanesthesia care unit (18). Moreover, it has been shown that elderly surgical patients who have had a perioperative pulmonary complication have increased mortality, particularly in the first three months after surgery (19). For these reasons, all attempts should be made to prevent perioperative hypoxemia and particularly during the induction period.

In conclusion, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management.

Back to Top | Article Outline


1. Marshall BE, Wyche MQ. Hypoxemia during and after anesthesia. Anesthesiology 1972; 37: 178–209.
2. Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia: an observer study. Br J Anaesth 1991; 66: 437–44.
3. Hedenstierna G, Tokics L, Strandberg A, et al. Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis. Acta Anaesthesiol Scand 1986; 30: 183–91.
4. Neumann P, Rothen HU, Berglund JE, et al. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 1999; 43: 295–301.
5. Tokics L, Hedenstierna G, Strandberg A, et al. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987; 66: 157–67.
6. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985; 62: 422–8.
7. Lundquist H, Hedenstierna G, Strandberg A, et al. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995; 36: 626–32.
8. Rothen HU, Sporre B, Englberg G, et al. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993; 71: 788–95.
9. Reber A, Englberg G, Wegenius G, Hedenstierna G. Lung aeration: the effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia 1996; 51: 733–7.
10. Rothen HU, Sporre B, Englberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345: 1387–91.
11. Rothen HU, Sporre B, Englberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.
12. Edmark L, Enlund M, Kostova-Aherdan K, Hedenstierna G. Atelectasis formation and apnoea tolerance after pre-oxygenation with 100%, 80%, or 60% oxygen. Anesthesiology 2001; 95: A1330.
13. Ho-Tai LM, Devitt JH, Noel AG, O’Donnell MP. Gas leak and gastric insufflation during controlled ventilation: face mask versus laryngeal mask airway. Can J Anaesth 1998; 45: 206–11.
14. Vyas H, Milner AD, Hopkin IE. Face mask resuscitation: does it lead to gastric distension? Arch Dis Child 1983; 58: 373–5.
15. Strandberg A, Tokics L, Brismar B, et al. Constitutional factors promoting development of atelectasis during anaesthesia. Acta Anaesthesiol Scand 1987; 31: 21–4.
16. Eichenberger A-S, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg 2002; 95: 1788–92.
17. Bindslev L, Hedenstierna G, Santesson J, et al. Ventilation-perfusion distribution during inhalation anaesthesia: effects of spontaneous breathing, mechanical ventilation and positive end-expiratory pressure. Acta Anaesthesiol Scand 1981; 25: 360–71.
18. Cote CJ, Goldstein EA, Cote MA, et al. A single-blind study of pulse oximetry in children. Anesthesiology 1988; 68: 184–8.
19. Manku K, Bacchetti P, Leung JM. Prognostic significance of postoperative in-hospital complications in elderly patients. I. Long-term survival. Anesth Analg 2003; 96: 583–9.
© 2003 International Anesthesia Research Society