Atelectasis occurs regularly during general anaesthesia, persists postoperatively and may contribute to significant morbidity and additional healthcare costs [1-3]. The resulting impairment of gas exchange and the increased intrapulmonary shunt correlate with atelectasis formation in the postoperative period. Atelectasis can be detected by computed tomography, but may only be seen on standard chest X-ray when it becomes massive [4-6]. In 85-90% of anaesthetized patients, densities can be found in the dependent parts of the lungs within a few minutes after induction of anaesthesia . Their development is independent of the type of anaesthesia (intravenous or inhalational), whether the patient is breathing spontaneously or is paralysed and mechanically ventilated . The magnitude of pulmonary shunt correlates well with the size of atelectasis . An interesting pathophysiological finding is that neither the atelectasis nor the shunt increases with the age of the patient . Atelectasis can persist for 2 days after major surgery , but usually disappears within 24 h in non-obese subjects following laparoscopy . Thus, it appears that the early formation of atelectasis and pulmonary shunt are an unavoidable 'adverse effect' of general anaesthesia .
As atelectasis may be one of the major causes of postoperative pulmonary complications and a predisposing factor for the development of hypoxaemia and nosocomial pneumonia, its prevention may be considered as an important objective in perioperative management [12,13]. A vital capacity manoeuvre has been proposed as an adjunct to conventional mechanical ventilation during general anaesthesia to forestall atelectasis and to reverse alveolar derecruitment maintaining functional residual capacity [14-16]. A vital capacity manoeuvre is defined as a short increase in airway pressure with the objective to open atelectatic alveoli and to stabilize them by a positive end-expiratory pressure set above the critical alveolar closing pressure, thus reversing derecruitment and the deterioration in compliance and gas exchange [17-19].
While vital capacity manoeuvres have become a relatively common clinical practice in managing patients with acute lung injury, particularly after suspected derecruitment, e.g. endotracheal suctioning , the beneficial effect of this intervention during general anaesthesia remains still a matter of dispute. In the following article we describe the pathogenesis of atelectasis in the perioperative period and discuss recent published investigations on the suitability of the vital capacity manoeuvre for the prevention of atelectasis during general anaesthesia.
Pulmonary atelectasis may be caused by a variety of factors, which have been classified into three basic mechanisms. Compression atelectasis occurs when the transmural pressure distending the alveolus is reduced. Absorption atelectasis occurs when less gas enters the alveolus than is removed by uptake by the blood. Loss-of-surfactant atelectasis occurs when the surface tension of an alveolus increases because of reduced surfactant concentration . In the perioperative period compression and absorption are the two major mechanisms for the occurrence of atelectasis.
Recent studies have made the explanation of atelectasis formation during anaesthesia more complex. On the one hand positive end-expiratory pressure can reopen collapsed lung tissue but as soon as positive end-expiratory pressure is discontinued atelectasis reappears within 1 min . The rapid formation of atelectasis after induction of anaesthesia and its discontinuation after applying adequate positive end-expiratory pressure may suggest that a major cause of atelectasis is compression of lung tissue rather than absorption of gas behind occluded airways . These results are confirmed by the fact that atelectasis could be reduced by phrenic nerve stimulation, as induced by the use of ketamine which does not promote atelectasis formation and maintains functional residual capacity during general anaesthesia [21,22]. However, after muscle relaxation and commencement of mechanical ventilation, atelectasis and intrapulmonary shunt developed despite the use of ketamine . These findings indicate that the loss of inspiratory muscle tone during muscle relaxation is an important pathogenetic factor in the occurrence of atelectasis. Thus, the greater abdominal pressure is more easily transmitted into the thoracic cavity when the diaphragm has a reduced muscle tone or is paralysed, as during general anaesthesia . On the other hand it has been demonstrated that when the lungs are ventilated with pure oxygen they rapidly re-collapse following a vital capacity manoeuvre . When the lungs are ventilated with 40% oxygen in nitrogen after the re-expansion, they remain open with no or only little atelectasis formation for half an hour or longer. These observations emphasize the importance of the inspired oxygen fraction (FiO2) suggesting that the rate of absorption of gas from the alveoli play an important role in the formation of atelectasis .
In this connection the question arises as to the necessity of preventing atelectasis during general anaesthesia, as most of the intraoperative atelectasis disappears within 24 h postoperatively and has no long-lasting effects . Nevertheless, it should be kept in mind that the major factors for the incidence of postoperative pulmonary complications do not depend on the type of anaesthesia, but on the type and the duration of surgery [25,26]. Surgery close to the diaphragm, such as major upper abdominal surgery, oesophagectomy or cardiothoracic surgery, is associated with a higher incidence of postoperative pulmonary complications than surgery in regions distant to the diaphragm . Operative procedures lasting longer than 3 h may be considered as an independent risk factor for the occurrence of postoperative pulmonary complications . In clinical studies on atelectasis, postoperative pulmonary complications and pneumonia are often considered together because the changes associated with atelectasis may predispose to nosocomial pneumonia. A continuum exists from non-infectious postoperative pulmonary complications (atelectasis) to infectious postoperative pulmonary complications (exacerbation of chronic bronchitis or pneumonia) . Despite the lack of direct evidence of a correlation between atelectasis and pneumonia, preventing atelectasis formation may be considered as a major factor in the reduction of postoperative pulmonary complications, particularly in patients at risk such as obese patients and patients undergoing major abdominal or cardiothoracic surgery [24,25].
Lachmann recommended a recruitment manoeuvre for opening collapsed lungs by applying high levels of peak inspiratory pressure for a short time and maintaining alveoli open by subsequent levels of positive end-expiratory pressure . An important principle of lung recruitment is that the pressures required to reopen an alveolus are considerably higher than those required to keep it from closing again. Theoretically, once these units are open, their mechanical properties change so that they may remain open for an undetermined period of time. This can be derived from the law of LaPlace (P = 2γ/r, where P is the alveolar pressure, γ the surface tension, and r the radius of the alveolus) such that the pressure necessary to keep the alveoli open is smaller at normal functional residual capacity. For that reason recruited alveolar units require less pressure to remain open. As lung recruitment with reopening of collapsed or closed lung parenchyma is an inspiratory, and not an expiratory phenomenon, a key issue is that sufficient positive end-expiratory pressure is applied to maintain the lung recruited .
Prevention of atelectasis: The role of vital capacity manoeuvre and positive end-expiratory pressure
In 1963 Bendixen and colleagues suggested that periodic deep breaths prevented progressive atelectasis formation and intrapulmonary shunting . In contrast to critically ill patients, studies concerning the vital capacity manoeuvre during general anaesthesia investigated patients with healthy lungs. Regarding this issue we have to question what are the main factors for the effectiveness of a vital capacity manoeuvre. First, the level and the duration of the applied recruitment pressure are of major importance for the responsiveness to a vital capacity manoeuvre [15,29]. Atelectasis is not affected by an increase in airway pressure of up to 20 cmH2O . Greaves and colleagues reported that an inspiratory pressure of at least 30 cmH2O was required to recruit approximately half of the initial atelectatic lung tissue of healthy lungs . Rothen and colleagues demonstrated that an inflation pressure of 40 cmH2O held for 15 s was required for a complete recruitment of all collapsed lung tissue of previously healthy individuals undergoing 20 min of general anaesthesia . Most of the re-expanded lung tissue remained inflated for at least 40 min after the vital capacity manoeuvre [30,31]. In a more recently published study, Rothen and colleagues suggested that this manoeuvre needs to be maintained only for 7-8 s in order to re-expand all previously collapsed lung tissue . These results were confirmed by Tusman and colleagues who reported significant improvement in oxygenation during the whole study period of 2 h after a vital capacity manoeuvre. Median arterial partial pressures of oxygen (PaO2) obtained at baseline were 20.4 kPa and increased to 25.4 kPa after the vital capacity manoeuvre, which was performed by an increase of positive end-expiratory pressure in steps of 5 cmH2O up to a maximum of 15 cmH2O and a tidal volume of 18 mL kg−1 or a peak inspiratory pressure of 40 cmH2O was reached. The setting was maintained for 10 breaths and was followed by a low positive end-expiratory pressure of 5 cmH2O. The increase in arterial oxygenation after the vital capacity manoeuvre suggested a reversal of anaesthesia-induced atelectasis and ventilation/perfusion mismatch. These findings indicate that pressures beyond the opening pressure of collapsed alveoli are necessary to overcome collapse of lung tissue, and that a positive end-expiratory pressure of at least 5 cmH2O is necessary to prevent derecruitment of the re-opened alveoli. Treatment with a positive end-expiratory pressure of 5 cmH2O alone, however, did not improve oxygenation . The same method was also successful in augmenting arterial oxygenation during one-lung ventilation .
Although the vital capacity manoeuvre has been well investigated in lung function studies in anaesthetized subjects, such a manoeuvre can be regarded as risky and may cause barotrauma [34,35]. The safety of a vital capacity manoeuvre has been questioned, but up to now no adverse haemodynamic effects or pulmonary complications have been reported.
It is known that high oxygen concentrations cause absorption atelectasis. Rothen and colleagues demonstrated that the use of a fraction of inspired oxygen of 100% for ventilating lungs after a vital capacity manoeuvre caused a re-development of atelectasis within 5 min after the recruitment manoeuvre, while ventilating lungs with 40% oxygen mixed with nitrogen delayed the development of alveolar collapse . In this context, Hedenstierna and colleagues suggested a lowering of oxygen fraction from 100% to 80% during induction of anaesthesia which does not shorten the safety time of the apnoea period which is particularly useful for difficult intubation, but reduces the amount of atelectasis . In a recently published study, Edmark and colleagues investigated the effects of 100%, 80% and 60% oxygen applied for 5 min during induction of anaesthesia on the formation of atelectasis and the fall in arterial oxygen saturation during apnoea. The corresponding times (mean ± standard deviation) to reach 90% oxygen saturation were 411 ± 84, 303 ± 59 and 213 ± 69 s, respectively . For safety reasons, it is common to ventilate patients with 100% oxygen during the induction of anaesthesia. In daily routine practice we have to consider carefully the risk benefit ratio between a small amount of atelectasis with mean values of less than 10 cm2[11,37] and the significant shortening of the time margin before unacceptable desaturation occurs. Benoit and colleagues demonstrated in patients ventilated with 100% oxygen at the end of surgery that an additional vital capacity manoeuvre performed 10 min before tracheal extubation lead only to a small reduction of atelectasis from 8.3% ± 6.2% to 6.8 ± 3.4% of the total lung area . However, Neumann and colleagues showed that the application of a positive end-expiratory pressure level of 10 cmH2O reduced atelectasis formation after a vital capacity manoeuvre even when an inspired oxygen fraction of 100% was applied. These authors suggested that a vital capacity manoeuvre followed by ventilation with positive end-expiratory pressure of 10 cmH2O should be considered whenever gas exchange is impaired and a patient is ventilated with high oxygen concentrations during general anaesthesia . Thus, atelectasis is most likely caused by a combination of lung compression and absorption of gas from poorly ventilated lung areas. This study group was the first to apply an active re-expansion manoeuvre combined with stabilization of the newly recruited alveoli by positive end-expiratory pressure during general anaesthesia. They concluded that ventilation by a pressure limited mode, as suggested by Lachmann and colleagues, might have opened alveoli more effectively and that the improvement in oxygenation could have been greater with a recruitment pressure of >40 cmH2O [15,17].
In a recently published study, Tusman and colleagues investigated the impact of an alveolar recruitment strategy on the amount and distribution of atelectasis in children by using magnetic resonance imaging . The alveolar vital capacity manoeuvre was performed by manually ventilating the lungs with a peak airway pressure of 40 cmH2O and a positive end-expiratory pressure of 15 cmH2O for 10 breaths. He found that the frequency of atelectasis was much less following the alveolar recruitment strategy compared with children who did not have the vital capacity manoeuvre performed. Furthermore this study showed - similar to adults - that the mere application of 5 cmH2O of positive end-expiratory pressure without prior recruitment did not show the same treatment effect and showed no difference compared to the control group without positive end-expiratory pressure.
In cardiac surgery with the use of cardiopulmonary bypass, impaired pulmonary gas exchange is a major problem in the perioperative period [41,42]. Though the cause of impairment of lung function is multifactorial, the development of atelectasis is proposed as the major contributing factor in the development of impaired gas exchange following cardiopulmonary bypass as the occurrence of atelectasis is exacerbated by the physical collapse of the lungs. In an animal study, extensive atelectasis 1 h after cardiopulmonary bypass correlated well with intrapulmonary shunt . In human beings, prominent atelectasis in the dependent lung areas has been described on the first postoperative day after cardiac surgery . Magnusson and colleagues demonstrated in an animal model, that post-cardiopulmonary bypass atelectasis can be effectively prevented by a vital capacity manoeuvre performed by inflating the lungs with a recruiting pressure of 40 cmH2O for 15 s at the end of cardiopulmonary bypass. Furthermore this study showed that vital capacity manoeuvre had no effect on intrapulmonary shunt when the pigs were ventilated with 100% oxygen . Studies in patients reported the reduction of development of intrapulmonary shunting and hypoxaemia after coronary artery bypass grafting by the performance of a vital capacity manoeuvre after termination of cardiopulmonary bypass  and earlier extubation of cardiac surgery patients who received a vital capacity manoeuvre at the end of cardiopulmonary bypass (6.5 ± 2.1 vs. 9.4 ± 4.2 h) .
A recently published study by Claxton and colleagues investigated the effects of an alveolar recruitment strategy on arterial oxygenation in 78 patients after cardiopulmonary bypass . The recruitment group received a pressure-controlled stepwise increase in positive end-expiratory pressure up to 15 cmH2O and tidal volumes up to 18 mL kg−1 until a peak inspiratory pressure of 40 cmH2O was reached, as performed by Tusman in a previous study . After the vital capacity manoeuvre, a low positive end-expiratory pressure level of 5 cmH2O was maintained until extubation on the intensive care unit. The authors observed only a temporary improvement in oxygenation in the recruitment group at 30 min and 1 h post bypass compared with the control groups who received either no positive end-expiratory pressure or a positive end-expiratory pressure of 5 cmH2O. However, there was no significant difference in any of the groups beyond 1 h. Dyhr and colleagues examined the effects of a lung vital capacity manoeuvre with or without a subsequently applied positive end-expiratory pressure in cardiac surgery patients. In this prospective, randomized and controlled study the authors showed that a positive end-expiratory pressure set 1 cmH2O above the lower inflection point is required after a lung vital capacity manoeuvre in patients ventilated with a high inspired fraction of oxygen to maintain lung volumes and the improved oxygenation. In the positive end-expiratory pressure group PaO2 increased from 34.5 ± 13 kPa to 50.6 + 12 kPa at 30 min after the lung vital capacity manoeuvre and was maintained at this level until the end of the study period. However, a lung vital capacity manoeuvre without subsequently applied positive end-expiratory pressure proved to be a useless tool for increasing lung volume and improving gas exchange . Thus, it appears that while a vital capacity manoeuvre might be helpful in reopening the lung a sustained effect requires an adequate positive end-expiratory pressure level.
It remains controversial to assume that the mere application of an appropriate positive end-expiratory pressure is sufficient for improving post-bypass pulmonary dysfunction in cardiac surgery patients. In an animal study, Magnusson and colleagues reported that the application of continuous positive airway pressure with 5 cmH2O during cardiopulmonary bypass was not effective in preventing post-cardiopulmonary bypass atelectasis and consequently impairment of oxygenation . In contrast, Loeckinger and colleagues showed that the application of continuous positive airways pressure with 10 cmH2O during cardiopulmonary bypass resulted in significantly improved gas exchange .
Furthermore, it has to be determined if patients at risk of developing atelectasis and postoperative pulmonary complications, who are ventilated with an appropriate positive end-expiratory pressure will benefit or even require a vital capacity manoeuvre. Morbidly obese patients have a higher incidence of postoperative pulmonary complications because functional residual capacity is lower, the alveolar-arterial gradient is increased and intra-abdominal pressure is higher [52,53]. Atelectasis in these patients develops not only more frequently, but also persists longer compared with non-obese patients . Coussa and colleagues demonstrated that the application of a positive end-expiratory pressure of 10 cmH2O during induction of anaesthesia was effective in preventing atelectasis formation in obese patients . Pelosi and colleagues reported that in morbidly obese patients mechanical ventilation with a positive end-expiratory pressure of 10 cmH2O compared to zero end-expiratory pressure resulted in a significantly higher blood partial pressure of oxygen (218 ± 47 vs. 110 ± 30 kPa) together with a lower elastance of the respiratory system (16.4 ± 3.6 vs. 26.8 ± 4.2 cmH2O L−1) . Furthermore this study showed that during general anaesthesia and paralysis the application of positive end-expiratory pressure improved respiratory function in morbidly obese patients, but not in normal subjects. Thus, application of a positive end-expiratory pressure of 10 cmH2O can be recommended in obese patients to forestall intraoperative atelectasis and to maintain functional residual capacity. However, at the current state of knowledge it is unknown if morbidly obese patients may profit from an additional vital capacity manoeuvre.
The mere application of a positive end-expiratory pressure of 10 cmH2O without a concomitant vital capacity manoeuvre has been investigated in several clinical studies and will consistently reopen collapsed lung tissue [5,8,37,55,56]. However, some atelectasis persists in most patients. Further increases of positive end-expiratory pressure may reopen these lung tissues with consecutive improvement of the ventilation/perfusion matching. On the other hand we have to balance the price we have to pay for a fully recruited lung achieved by a vital capacity manoeuvre with the application of adequate positive end-expiratory pressure levels. Increasing positive end-expiratory pressure may have undesired consequences, as worsening the ventilation perfusion mismatch redirects blood flow from well-ventilated lung units to dependant lung areas increasing ventilatory dead space and maintaining intrapulmonary shunt . The increased intrathoracic pressure impedes right atrial filling, decreases cardiac output and depresses oxygen delivery when compensatory mechanisms fail to maintain the gradient of vascular pressure that drives venous return. Consequently, splanchnic, hepatic and renal perfusion decrease and might lead to an impairment of organ function. Therefore we have to keep in mind the risk benefit ratio between optimization of gas exchange and haemodynamic side effects.
Most investigations concerning a vital capacity manoeuvre were performed with a rather low positive end-expiratory pressure setting in both study and control groups. In contrast, it has been shown that the beneficial effects of a vital capacity manoeuvre without the subsequent application of an adequate positive end-expiratory pressure are only transient. Thus it remains to be determined what the gain of a vital capacity manoeuvre would be to patients at risk who are ventilated with a higher positive end-expiratory pressure setting throughout anaesthesia. Further studies will be needed to determine if the improvement in oxygenation is followed by a decrease of postoperative pulmonary complications and an improvement of clinical outcome.
Regarding the current state of literature, a vital capacity manoeuvre during general anaesthesia cannot be generally recommended and may only be useful under specific circumstances when mechanical ventilation with a high inspiratory fraction of oxygen is required or during cardiac surgery at the end of cardiopulmonary bypass to reduce the amount of atelectasis and to maintain adequate gas exchange.
1. Lindberg P, Gunnarsson L, Tokics L, et al.
Atelectasis and lung function in the postoperative period. Acta Anaesthesiol Scand
2. Lawrence VA, Hilsenbeck SG, Mulrow CD, et al.
Incidence and hospital stay for cardiac and pulmonary complications after abdominal surgery. J Gen Intern Med
3. Lam WW, Chen PP, So NM, Metreweli C. Sedation versus general anaesthesia in paediatric patients undergoing chest CT. Acta Radiol
4. Prys-Roberts C, Nunn JF, Dobson RH, Robinson RH, Greenbaum R, Harris RS. Radiologically undetected pulmonary collapse in the supine position. Lancet
5. Brismar B, Hedenstierna G, Lundquist H, et al.
Pulmonary densities during anaesthesia with muscular relaxation - a proposal of atelectasis. Anesthesiology
6. Lundquist H, Hedenstierna G, Strandberg A, Tokics L, Brismar B. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol
7. Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Atelectasis during anaesthesia and in the post-operative period. Acta Anaesthesiol Scand
8. Tokics L, Hedenstierna G, Strandberg A, Brismar B, Lundquist H. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology
9. Gunnarsson L, Tokics L, Gustavsson H, Hedenstierna G. Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. Br J Anaesth
10. Eichenberger AS, Proietti S, Wicky S, et al.
Morbid obesity and postoperative atelectasis: an underestimated problem. Anesth Analg
11. Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G. Atelectasis and pulmonary shunting during induction of general anaesthesia - can they be avoided? Acta Anaesthesiol Scand
12. Hedenstierna G. Atelectasis and its prevention during anaesthesia. Eur J Anaesthesiol
13. Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth
14. Crotti S, Mascheroni D, Caironi P, et al.
Recruitment and derecruitment during acute respiratory failure. A clinical study. Am J Respir Crit Care Med
15. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia: a computed tomographic study. Br J Anaesth
16. Tusman G, Böhm SH, Vazquez de Anda GF, do Campo JL, Lachmann B. 'Alveolar recruitment strategy' improves arterial oxygenation during general anaesthesia. Br J Anaesth
17. Lachmann B. Open up the lung and keep the lung open. Intensive Care Med
18. Bond DM, McAloon J, Froese AB. Sustained inflations improve respiratory compliance during high frequency oscillatory ventilation but not during large tidal volume positive pressure ventilation in rabbits. Crit Care Med
19. Richard JC, Maggiore S, Mercat A. Where are we with recruitment maneuvers in patients with acute lung injury and acute respiratory distress syndrome? Curr Opin Crit Care
20. Arnold JH. To recruit or not derecruit: that is the question. Crit Care Med
21. Hedenstierna G, Tokics L, Lundquist H, Andersson T, Strandberg A, Brismar B. Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis. Anesthesiology
22. Tokics L, Strandberg A, Brismar B, Lundquist H, Hedenstierna G. Computerized tomography of the chest and gas exchange measurements during ketamine anaesthesia. Acta Anaesthesiol Scand
23. Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a re-expansion maneuver during general anesthesia. Anesthesiology
24. Tseuda K, Debrand M, Bivins BA, Wright BD, Griffen WO. Pulmonary complications in the morbidly obese following jejunoileal bypass surgery under narcotic anesthesia. Int Surg
25. Kroenke K, Lawrence VA, Theroux JF, Tuley MR. Operative risk in patients with severe obstructive pulmonary disease. Arch Intern Med
26. Pedersen T, Eliasen K, Henriksen E. A prospective study of risk factors and cardiopulmonary complications associated with anaesthesia and surgery: risk indicators of cardiopulmonary morbidity. Acta Anaesthesiol Scand
27. Vazquez de Anda GF, Lachmann B. Protecting the lung during mechanical ventilation with the open lung concept. Acta Anaesthesiol Scand
1998; 112 (Suppl):
28. Bendixen HH, Hedley-Whyte J, Laver MB. Improved oxygenation in surgical patients during general anesthesia with controlled ventilation. N Engl J Med
29. Greaves IA, Hildebrandt J, Hoppin FG. Micromechanics of the lung. In: Macklem PT, Mead J, Bethesda MD, eds. Handbook of Physiology. American Society of Physiology
30. Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G. Prevention of atelectasis during general anaesthesia. Lancet
31. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand
32. Rothen HU, Neumann P, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Dynamics of re-expansion of atelectasis during general anaesthesia. Br J Anaesth
33. Tusman G, Böhm SH, Melkun F, et al.
Alveolar recruitment strategy increases arterial oxygenation during one-lung ventilation. Ann Thorac Surg
34. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema: respective effects of high airway pressure. Am Rev Respir Dis
35. Dreyfuss D, Saumon G. Barotrauma is volutrauma, but which volume is the one responsible? Intensive Care Med
36. Hedenstierna G, Edmark L, Aherdan KK. Time to reconsider the pre-oxygenation during induction of anaesthesia. Minerva Anesthesiol
37. Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology
38. Benoit Z, Wicky S, Fischer JF, et al.
The effect of increased Fi
before tracheal extubation on postoperative atelectasis. Anesth Analg
39. Neumann P, Rothen HU, Berglund JE, Valtysson A, Magnusson A, Hedenstierna G. Positive endexpiratory pressure prevents atelectasis during general anesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand
40. Tusman G, Böhm ST, Tempra A, et al.
Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology
41. Hachenberg T, Tenling A, Nystrom SO, Tyden H, Hedenstierna G. Ventilation-perfusion inequality in patients undergoing cardiac surgery. Anesthesiology
42. Cox CM, Ascione R, Cohen AM, Davies IM, Ryder IG, Angelini GD. Effect of cardiopulmonary bypass on pulmonary gas exchange: a prospective randomized study. Ann Thorac Surg
43. Magnusson L, Zemgulis V, Wicky S, Tyden H, Thelin S, Hedenstierna G. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology
44. Tenling A, Hachenberg T, Tyden H, Wegenius G, Hedenstierna G. Atelectasis and gas exchange after cardiac surgery. Anesthesiology
45. Magnusson L, Zemgulis V, Tenling A, et al.
Use of vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study. Anesthesiology
46. Tschernko EM, Bambazek A, Wisser W, et al.
Intrapulmonary shunt after cardiopulmonary bypass: the use of vital capacity maneuvers versus off-pump coronary artery bypass grafting. J Thorac Cardiovasc Surg
47. Murphy GS, Szokol JW, Curran RD, Votapka TV, Vender JS. Influence of vital capacity maneuver on pulmonary gas exchange after cardiopulmonary bypass. J Cardiothorac Vasc Anesth
48. Claxton BA, Morgan P, McKeague H, Mulpur A, Berridge J. Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia
49. Dyhr T, Laursen N, Larsson A. Effects of lung vital capacity maneuver and positive end-expiratory pressure on lung volume, respiratory mechanics and alveolar gas mixing in patients ventilated after cardiac surgery. Acta Anaesthesiol Scand
50. Magnusson L, Zemgulis V, Wicky S, Tyden H, Hedenstierna G. Effect of CPAP during cardiopulmonary bypass on postoperative function. An experimental study. Acta Anaesthesiol Scand
51. Loeckinger A, Kleinsasser A, Lindner KH, Margreiter J, Keller C, Hoermann C. Continuous positive airway pressure at 10 cmH2
O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg
52. Pelosi P, Croci M, Ravagnan I, et al.
Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol
53. Pelosi P, Croci M, Ravagnan I, et al.
The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg
54. Coussa M, Proietti S, Frascarolo P, Spahn D, Magnusson L. Continuous positive airway pressure prevents atelectasis formation during induction of general anaesthesia in morbidly obese patients. Swiss Med Wkly
55. Pelosi P, Ravagnan I, Giurati G, et al.
Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology
56. D'Angelo E, Calderini E, Tavola M, Bono D, Milic-Emili J. Effect of PEEP on respiratory mechanics in anesthetized paralyzed humans. J Appl Physiol
57. Santesson J. Oxygen transport and venous admixture in the extreme obese: influence of anaesthesia and artificial ventilation with and without positive end-expiratory pressure. Acta Anaesthesiol Scand