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Anesth Analg 2002;95:1777-1781 © 2002 International Anesthesia Research Society
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Abstract |
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General anesthesia promotes pulmonary atelectasis, which can be eliminated by a vital capacity (VC) maneuver (inflation of the lungs to 40 cm H2O for 15 s). High-inspired oxygen concentration favors recurrence of atelectasis. Therefore, 100% oxygen before tracheal extubation may contribute to atelectasis. To evaluate whether the use of 100% oxygen before extubation increases the amount of postoperative atelectasis, we studied 30 adults scheduled for elective surgery of the extremities. Ten minutes before the presumed end of surgery, patients were randomly assigned to (a) a fraction of inspired oxygen (FIO2) = 1.0 (n = 10), (b) VC maneuver + FIO2 = 1.0 (n = 10), or (c) VC maneuver + FIO2 = 0.4 (n = 10). The amount of atelectasis was measured by computed tomography scan, and oxygenation was studied by arterial blood gas analysis. Data were analyzed by one-way analysis of variance with Bonferroni correction. Results are presented as mean ± SD; P < 0.05 was considered significant. In the VC maneuver + FIO2 = 0.4 group, postoperative atelectasis was smaller (2.6% ± 1.1% of total lung surface, P < 0.05) than in the FIO2 = 1.0 group (8.3% ± 6.2%) and in the VC maneuver + FIO2 = 1.0 group (6.8% ± 3.4%). Oxygen 100% at the end of general anesthesia promotes postoperative atelectasis. A safety margin in terms of oxygenation during tracheal extubation is essential, and further studies should therefore evaluate whether atelectasis formation could be prevented despite the use of 100% oxygen.
IMPLICATIONS: For safety reasons, it is common to ventilate patients with 100% oxygen before tracheal extubation. This study demonstrates that this practice favors postoperative atelectasis.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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General anesthesia 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 gas (FIO2) is used (9,10). A vital capacity (VC) maneuver (manual inflation of the intubated patient’s lungs to 40 cm H2O for 15 s) nearly eliminates atelectasis (8), which recurs within 5 minutes if the patient is ventilated with 100% oxygen (11). In contrast, with 40% oxygen, atelectasis reappears only partially after 45 minutes (12). Short periods of ventilation with 100% oxygen thus may favor atelectasis formation, presumably also before extubation.
The significance of postoperative atelectasis is not precisely known but may increase the risk of pulmonary infection. Moreover, atelectasis may cause the frequent incidence of hypoxemia (SpO2 <90%) seen in the early postoperative period (2). Therefore, avoiding postoperative atelectasis may be beneficial. The aim of this study was to assess whether the use of 100% oxygen before extubation favors postoperative atelectasis formation.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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After institutional ethics committee approval and written informed consent, 30 adults (Table 1) that were ASA status I and II, aged 18 to 64 yr old, with a body mass index <30, scheduled for elective surgery of the extremities in the supine position lasting <2.5 h were included in this prospective, randomized, double-blinded study. Patients were excluded if they were hospitalized more than 24 h before the operation or if they had a history or clinical signs of heart or lung disease.
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Patients were premedicated with midazolam 7.5 mg per os. After 3 min of breathing 100% oxygen by face mask, the induction was made with fentanyl 2 µg/kg and propofol 2 mg/kg and was followed by a continuous infusion of propofol 6–10 mg · kg-1 · h-1. Subsequent doses of fentanyl and the rate of propofol infusion were adjusted according to hemodynamic variables. Endotracheal intubation was facilitated by vecuronium 0.1 mg/kg IV, and additional doses were given if required. Until complete relaxation was achieved, patients were manually ventilated with 100% oxygen via a face mask. After intubation, the lungs were mechanically ventilated with a tidal volume of 10 mL/kg. The rate was adjusted to maintain an end-tidal CO2 pressure of approximately 30–35 mm Hg. During the maintenance of anesthesia, 40% oxygen in nitrogen was administered. The peripheral arterial oxygen saturation was monitored continuously by pulse oxymetry. No positive end-expiratory pressure was used.
Ten minutes before the presumed end of surgery, randomization was performed. In the Control group (n = 10), FIO2 was increased to 100%. In the VC Maneuver + FIO2 = 1.0 group (n = 10), the increase in FIO2 was preceded by the VC maneuver. In the VC Maneuver + FIO2 = 0.4 group (n = 10), after the VC maneuver, FIO2 was kept at 0.4.
Train-of-four response was controlled via a peripheral nerve stimulator. Ensuring a response of 4/4, neuromuscular block was reversed (neostigmine 2.5 mg and glycopyrronium 0.5 mg IV). When the patient was fully awake and spontaneously breathing, the trachea was extubated without any positive pressure. Patients were then transported to the computed tomography (CT) scan breathing room air. The peripheral arterial oxygen saturation was continuously monitored by pulse oxymetry. Should SpO2 have decreased to less than 94%, the patient would have been given supplemental oxygen. Postoperative pain management consisted of the residual effect of intraoperative fentanyl and propacetamol if required.
Atelectasis was measured with CT scan (7,8). Front scout view was obtained, and 3 sections of 5 mm at 120 kV and 150 mA were obtained at end-expiratory position (at functional residual capacity) at the level of the interventricular septum with a lung algorithm (GE LightSpeed, General Electric Company, Milwaukee, WI). The CT data were transferred on a GE Advantage Window Station (General Electric Company). For each patient, the interventricular septum CT section was selected. The interventricular septum 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 apex (13). Each right and left lung surfaces were manually extracted, and a window setting of -1000 to +100 Hounsfield Unit (HU) was selected to assess the total lung surface. A threshold of -1000 to -500 HU was applied to quantify the amount of normally ventilated lung, a second threshold of -500 to -100 HU was chosen to establish the surface of poorly ventilated lung, and a third threshold of -100 to +100 HU was set to measure the surface of atelectatic lung area (Fig. 1). The right and left lungs surface of atelectasis were summed and reported to the total lung surface. Only one investigator (SW) performed these measurements, and he was blinded to the randomization.
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Two arterial blood samples, obtained through radial artery puncture, were drawn on room air. One was before the induction of anesthesia, and one was on arrival in the recovery room.
Values are expressed as mean ± SD. Baseline results and atelectatic surface were compared by a one-way analysis of variance for continuous variables and with the 
2 for discrete variables. Comparison between groups for oxygenation was performed with a two-way analysis of variance for repeated measurements on one way (time). Bonferroni correction was used for multiple comparisons. P < 0.05 was considered significant.
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Results |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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Thirty-four patients were enrolled in the study. Four patients were excluded because the CT scan was not successful for the following reasons: extreme agitation in two patients, artifacts from osteosynthesis material in one patient, and technical failure in one patient. There was no difference among groups for sex, age, body mass index, duration of surgery, and the delay between randomization, extubation, and second measurements (Table 1). No patient received supplemental oxygen or narcotics after extubation until the end of the protocol.
Postoperative atelectatic surface in the VC Maneuver + FIO2 = 0.4 group was significantly smaller than in the two other groups (Figs. 2 and 3). There was no difference regarding oxygenation among the three groups at baseline. In contrast, postextubation PaO2 (Fig. 2) was significantly larger in the VC Maneuver + FIO2 = 0.4 group when compared with the VC Maneuver + FIO2 = 1.0 group but without a statistically significant difference compared with the FIO2 = 1.0 group.
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Discussion |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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The major finding of the present study is that the use of 100% oxygen at the end of general anesthesia promotes postoperative atelectasis regardless of whether a VC maneuver was performed at the end of anesthesia. In contrast, a VC maneuver followed by a FIO2 of 40% completely prevented postoperative atelectasis formation.
The method of atelectasis measurement by CT scan is established (7,8). To avoid excessive radiation exposure, only the level of the interventricular septum was chosen. For the same reason, and because atelectasis is not seen in healthy patients (3,9,11,14), no preoperative CT scan was performed.
In the two groups exposed to 100% oxygen, the duration of pure oxygen administration at the end of general anesthesia (approximately 20 minutes) was relatively long (Table 1). Indeed, in our institution, orthopedic patients are not tracheally extubated in the operating room but in the anesthesia room. This explains the delay between the end of surgery and tracheal extubation. It is possible that this long exposure to 100% oxygen is not representative for patients who are tracheally extubated directly in the operating room, and this might have produced a greater amount of atelectasis. However, previous investigators have shown that atelectasis reappears within 5 minutes after a VC maneuver if the FIO2 is 1.0 (12,15) and that the prolongation of 100% oxygen exposure (up to 40 minutes) is not associated with a significant further increase in the amount of atelectasis (12). It suggests that very short periods of pure oxygen ventilation already induce atelectasis.
The VC maneuver may cause barotrauma and certainly reduces the cardiac output for the time period of inflation. The safety of this procedure concerning parenchymal trauma has been demonstrated in an animal model (16). Furthermore, this maneuver has now been used in more than 500 patients during various studies without any adverse effect. Moreover, the VC maneuver can be shortened to seven to eight seconds (17), which certainly reduces the hemodynamic consequences without altering the efficacy.
Inflation of the lungs to an airway pressure of 40 cm H2O corresponds closely to the VC measured before anesthesia in the same subjects (8). Therefore, volutrauma should not be a concern.
The choice of the two FIO2 studied was guided by the practice in many institutions that is to ventilate during anesthesia with 40% oxygen and to increase it to 100% just before tracheal extubation. In one investigation (18), no difference was found in postoperative atelectasis in patients ventilated with 30% or 80% oxygen. But in this study, all patients were ventilated with 100% oxygen at the induction of anesthesia, and no VC maneuver was performed. Therefore, the postoperative atelectasis observed could be the result of atelectasis that appeared during the induction.
A correlation has been shown between atelectasis and shunt (3,4) and between atelectasis and PaO2 (3,17); consequently, PaO2 should be directly affected by atelectasis. Our study failed to demonstrate any difference in postoperative oxygenation between the FIO2 = 1.0 group and VC Maneuver + FIO2 = 0.4 group, despite the tendency of higher PaO2 values in the latter group. One patient in the FIO2 = 1.0 group showed a PaCO2 of 23.5 mm Hg, suggesting acute hyperventilation (pain?) or air contamination of the blood sample. In contrast, all other patients in the study had PaCO2 values higher than 32 mm Hg. When repeating the statistical analysis without this outlier patient (highest PaO2 of all patients, 120.8 mm Hg), the PaO2 value in the VC Maneuver + FIO2 = 0.4 group became significantly higher than in the FIO2 = 1.0 group.
We evaluated the amount of atelectasis in the immediate postoperative period. One could argue that in most patients, after some hours, atelectasis may disappear after some deep breaths. However, it has been shown that lung collapse may persist for one to four days in some patients (11). Nevertheless, atelectasis, even for a short period, may contribute to the frequent incidence of hypoxemia observed in the early postoperative period (2). Moreover, particularly in patients at risk, such as the morbidly obese, atelectasis may also contribute to later pulmonary complications such as pneumonia. In conclusion, 100% oxygen at the end of general anesthesia favors postoperative atelectasis formation. During anesthesia, recurrence of atelectasis after a VC maneuver can be prevented by the application of 10 cm H2O of positive end-expiratory pressure in the presence of high-inspired oxygen concentration (15). To keep the benefits of enhancing the oxygen stores at the critical time of tracheal extubation, we suggest further studies to assess if postoperative atelectasis could be prevented by the same maneuver, or others, realized before tracheal extubation.
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References |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionReferences |
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- Marshall BE, Wyche MQ Jr. Hypoxemia during and after anesthesia. Anesthesiology 1972; 37: 178–209.[Web of Science][Medline]
- Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia: an observer study. Br J Anaesth 1991; 66: 437–44.
[Abstract/Free Full Text] - 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.[Web of Science][Medline]
- 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.[Web of Science][Medline]
- Rothen HU, Sporre B, Engberg G, et al. Airway closure, atelectasis and gas exchange during general anaesthesia. Br J Anaesth 1998; 81: 681–6.
[Abstract/Free Full Text] - Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985; 62: 422–8.[Web of Science][Medline]
- 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.[Web of Science][Medline]
- Rothen HU, Sporre B, Engberg G, et al. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993; 71: 788–95.
[Abstract/Free Full Text] - Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345: 1387–91.[Web of Science][Medline]
- Reber A, Engberg G, Wegenius G, et al. Lung aeration: the effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia 1996; 51: 733–7.[Web of Science][Medline]
- Lindberg P, Gunnarsson L, Tokics L, et al. Atelectasis and lung function in the postoperative period. Acta Anaesthesiol Scand 1992; 36: 546–53.[Web of Science][Medline]
- Rothen HU, Sporre B, Engberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.[Web of Science][Medline]
- Reber A, Engberg G, Sporre B, et al. Volumetric analysis of aeration in the lungs during general anaesthesia. Br J Anaesth 1996; 76: 760–6.
[Abstract/Free Full Text] - Rothen HU, Sporre B, Engberg G, et al. Atelectasis and pulmonary shunting during induction of general anaesthesia: can they be avoided? Acta Anaesthesiol Scand 1996; 40: 524–9.[Web of Science][Medline]
- 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.[Web of Science][Medline]
- Magnusson L, Tenling A, Lemoine R, et al. The safety of one, or repeated, vital capacity maneuvers during general anesthesia. Anesth Analg 2000; 91: 702–7.
[Abstract/Free Full Text] - Rothen HU, Neumann P, Berglund JE, et al. Dynamics of re-expansion of atelectasis during general anaesthesia. Br J Anaesth 1999; 82: 551–6.
[Abstract/Free Full Text] - Akca O, Podolsky A, Eisenhuber E, et al. Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology 1999; 91: 991–8.[Web of Science][Medline]
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