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Goran Hedenstierna - One of the best experts on this subject based on the ideXlab platform.
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higher age and obesity limit Atelectasis formation during anaesthesia an analysis of computed tomography data in 243 subjects
BJA: British Journal of Anaesthesia, 2020Co-Authors: Goran Hedenstierna, Hans Ulrich Rothen, Leif Tokics, Henrik Reinius, Erland Ostberg, John OhrvikAbstract:Abstract Background General anaesthesia is increasingly common in elderly and obese patients. Greater age and body mass index (BMI) worsen gas exchange. We assessed whether this is related to increasing Atelectasis during general anaesthesia. Methods This primary analysis included pooled data from previously published studies of 243 subjects aged 18–78 yr, with BMI of 18–52 kg m−2. The subjects had no clinical signs of cardiopulmonary disease, and they underwent computed tomography (CT) awake and during anaesthesia before surgery after preoxygenation with an inspired oxygen fraction (FIO2) of >0.8, followed by mechanical ventilation with FIO2 of 0.3 or higher with no PEEP. Atelectasis was assessed by CT. Results Atelectasis area of up to 39 cm2 in a transverse scan near the diaphragm was seen in 90% of the subjects during anaesthesia. The log of Atelectasis area was related to a quadratic function of (age+age2) with the most Atelectasis at ∼50 yr (r2=0.08; P Conclusions Atelectasis during general anaesthesia increased with age up to 50 yr and decreased beyond that. Atelectasis increased with BMI in normal and overweight patients, but showed no further increase in obese subjects (BMI ≥30 kg m−2). Therefore, greater age and obesity appear to limit Atelectasis formation during general anaesthesia.
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oxygen concentration and characteristics of progressive Atelectasis formation during anaesthesia
Acta Anaesthesiologica Scandinavica, 2011Co-Authors: Lennart Edmark, Erland Ostberg, Udo Auner, Mats Enlund, Goran HedenstiernaAbstract:Background: Atelectasis is a common consequence of pre-oxygenation with 100% oxygen during induction of anaesthesia. Lowering the oxygen level during pre-oxygenation reduces Atelectasis. Whether this effect is maintained during anaesthesia is unknown. Methods: During and after pre-oxygenation and induction of anaesthesia with 60%, 80% or 100% oxygen concentration, followed by anaesthesia with mechanical ventilation with 40% oxygen in nitrogen and positive end-expiratory pressure of 3 cmH2O, we used repeated computed tomography (CT) to investigate the early (0–14 min) vs. the later time course (14–45 min) of Atelectasis formation. Results: In the early time course, Atelectasis was studied awake, 4, 7 and 14 min after start of pre-oxygenation with 60%, 80% or 100% oxygen concentration. The differences in the area of Atelectasis formation between awake and 7 min and between 7 and 14 min were significant, irrespective of oxygen concentration (P<0.05). During the late time course, studied after pre-oxygenation with 80% oxygen, the differences in the area of Atelectasis formation between awake and 14 min, between 14 and 21 min, between 21 and 28 min and finally between 21 and 45 min were all significant (P<0.05). Conclusion: Formation of Atelectasis after pre-oxygenation and induction of anaesthesia is oxygen and time dependent. The benefit of using 80% oxygen during induction of anaesthesia in order to reduce Atelectasis diminished gradually with time.
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mechanisms of Atelectasis in the perioperative period
Best Practice & Research Clinical Anaesthesiology, 2010Co-Authors: Goran Hedenstierna, Lennart EdmarkAbstract:Atelectasis appears in about 90% of all patients who are anaesthetised. Up to 15–20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Atelectasis can persist for several days in the postoperative period. It is likely to be a focus of infection and may contribute to pulmonary complications. A major cause of anaesthesia-induced lung collapse is the use of high oxygen concentration during induction and maintenance of anaesthesia together with the use of anaesthetics that cause loss of muscle tone and fall in functional residual capacity (a common action of almost all anaesthetics). This causes absorption Atelectasis behind closed airways. Compression of lung tissue and loss of surfactant or surfactant function are additional potential causes of Atelectasis. Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue results in rapid reappearance of Atelectasis. If 40% O 2 in nitrogen is used for ventilation of the lungs, Atelectasis reappears slowly. A post-oxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening. However, a combination of oxygenation and airway suctioning will most likely cause new Atelectasis. Recruitment at the end of the anaesthesia followed by ventilation with 100% O 2 causes new Atelectasis before anaesthesia is terminated but not with ventilation with lower fraction of inspired oxygen (FIO 2 ). Thus, recruitment must be followed by ventilation with moderate FIO 2 .
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Atelectasis Formation During Anesthesia: Causes and Measures to Prevent It
Journal of Clinical Monitoring and Computing, 2000Co-Authors: Goran Hedenstierna, Hans Ulrich RothenAbstract:Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (Atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of Atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no Atelectasis. There are different procedures that can be used in order to prevent Atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and Atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H_2O, maintained for 7–8 seconds (recruitment or “vital capacity” manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of Atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of Atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO_2, e.g. 0.3–0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, Atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of Atelectasis. Finally, intermittent “vital capacity”-manoeuvres together with PEEP reduces the amount of Atelectasis and pulmonary shunt.
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Atelectasis Formation During Anesthesia: Causes and Measures to Prevent It
Journal of Clinical Monitoring and Computing, 2000Co-Authors: Goran Hedenstierna, Hans Ulrich RothenAbstract:Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (Atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of Atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no Atelectasis. There are different procedures that can be used in order to prevent Atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and Atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H_2O, maintained for 7–8 seconds (recruitment or “vital capacity” manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of Atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of Atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO_2, e.g. 0.3–0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, Atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of Atelectasis. Finally, intermittent “vital capacity”-manoeuvres together with PEEP reduces the amount of Atelectasis and pulmonary shunt.
Lennart Edmark - One of the best experts on this subject based on the ideXlab platform.
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oxygen concentration and characteristics of progressive Atelectasis formation during anaesthesia
Acta Anaesthesiologica Scandinavica, 2011Co-Authors: Lennart Edmark, Erland Ostberg, Udo Auner, Mats Enlund, Goran HedenstiernaAbstract:Background: Atelectasis is a common consequence of pre-oxygenation with 100% oxygen during induction of anaesthesia. Lowering the oxygen level during pre-oxygenation reduces Atelectasis. Whether this effect is maintained during anaesthesia is unknown. Methods: During and after pre-oxygenation and induction of anaesthesia with 60%, 80% or 100% oxygen concentration, followed by anaesthesia with mechanical ventilation with 40% oxygen in nitrogen and positive end-expiratory pressure of 3 cmH2O, we used repeated computed tomography (CT) to investigate the early (0–14 min) vs. the later time course (14–45 min) of Atelectasis formation. Results: In the early time course, Atelectasis was studied awake, 4, 7 and 14 min after start of pre-oxygenation with 60%, 80% or 100% oxygen concentration. The differences in the area of Atelectasis formation between awake and 7 min and between 7 and 14 min were significant, irrespective of oxygen concentration (P<0.05). During the late time course, studied after pre-oxygenation with 80% oxygen, the differences in the area of Atelectasis formation between awake and 14 min, between 14 and 21 min, between 21 and 28 min and finally between 21 and 45 min were all significant (P<0.05). Conclusion: Formation of Atelectasis after pre-oxygenation and induction of anaesthesia is oxygen and time dependent. The benefit of using 80% oxygen during induction of anaesthesia in order to reduce Atelectasis diminished gradually with time.
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mechanisms of Atelectasis in the perioperative period
Best Practice & Research Clinical Anaesthesiology, 2010Co-Authors: Goran Hedenstierna, Lennart EdmarkAbstract:Atelectasis appears in about 90% of all patients who are anaesthetised. Up to 15–20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Atelectasis can persist for several days in the postoperative period. It is likely to be a focus of infection and may contribute to pulmonary complications. A major cause of anaesthesia-induced lung collapse is the use of high oxygen concentration during induction and maintenance of anaesthesia together with the use of anaesthetics that cause loss of muscle tone and fall in functional residual capacity (a common action of almost all anaesthetics). This causes absorption Atelectasis behind closed airways. Compression of lung tissue and loss of surfactant or surfactant function are additional potential causes of Atelectasis. Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue results in rapid reappearance of Atelectasis. If 40% O 2 in nitrogen is used for ventilation of the lungs, Atelectasis reappears slowly. A post-oxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening. However, a combination of oxygenation and airway suctioning will most likely cause new Atelectasis. Recruitment at the end of the anaesthesia followed by ventilation with 100% O 2 causes new Atelectasis before anaesthesia is terminated but not with ventilation with lower fraction of inspired oxygen (FIO 2 ). Thus, recruitment must be followed by ventilation with moderate FIO 2 .
Hans Ulrich Rothen - One of the best experts on this subject based on the ideXlab platform.
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higher age and obesity limit Atelectasis formation during anaesthesia an analysis of computed tomography data in 243 subjects
BJA: British Journal of Anaesthesia, 2020Co-Authors: Goran Hedenstierna, Hans Ulrich Rothen, Leif Tokics, Henrik Reinius, Erland Ostberg, John OhrvikAbstract:Abstract Background General anaesthesia is increasingly common in elderly and obese patients. Greater age and body mass index (BMI) worsen gas exchange. We assessed whether this is related to increasing Atelectasis during general anaesthesia. Methods This primary analysis included pooled data from previously published studies of 243 subjects aged 18–78 yr, with BMI of 18–52 kg m−2. The subjects had no clinical signs of cardiopulmonary disease, and they underwent computed tomography (CT) awake and during anaesthesia before surgery after preoxygenation with an inspired oxygen fraction (FIO2) of >0.8, followed by mechanical ventilation with FIO2 of 0.3 or higher with no PEEP. Atelectasis was assessed by CT. Results Atelectasis area of up to 39 cm2 in a transverse scan near the diaphragm was seen in 90% of the subjects during anaesthesia. The log of Atelectasis area was related to a quadratic function of (age+age2) with the most Atelectasis at ∼50 yr (r2=0.08; P Conclusions Atelectasis during general anaesthesia increased with age up to 50 yr and decreased beyond that. Atelectasis increased with BMI in normal and overweight patients, but showed no further increase in obese subjects (BMI ≥30 kg m−2). Therefore, greater age and obesity appear to limit Atelectasis formation during general anaesthesia.
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Atelectasis Formation During Anesthesia: Causes and Measures to Prevent It
Journal of Clinical Monitoring and Computing, 2000Co-Authors: Goran Hedenstierna, Hans Ulrich RothenAbstract:Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (Atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of Atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no Atelectasis. There are different procedures that can be used in order to prevent Atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and Atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H_2O, maintained for 7–8 seconds (recruitment or “vital capacity” manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of Atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of Atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO_2, e.g. 0.3–0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, Atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of Atelectasis. Finally, intermittent “vital capacity”-manoeuvres together with PEEP reduces the amount of Atelectasis and pulmonary shunt.
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Atelectasis Formation During Anesthesia: Causes and Measures to Prevent It
Journal of Clinical Monitoring and Computing, 2000Co-Authors: Goran Hedenstierna, Hans Ulrich RothenAbstract:Pulmonary gas exchange is regularly impaired during general anaesthesia with mechanical ventilation. This results in decreased oxygenation of blood. A major cause is collapse of lung tissue (Atelectasis), which can be demonstrated by computed tomography but not by conventional chest x-ray. Collapsed lung tissue is present in 90% of all subjects, both during spontaneous breathing and after muscle paralysis, and whether intravenous or inhalational anaesthetics are used. There is a correlation between the amount of Atelectasis and pulmonary shunt. Shunt does not increase with age. In obese patients, larger atelectatic areas are present than in lean ones. Finally, patients with chronic obstructive lung disease may show less or even no Atelectasis. There are different procedures that can be used in order to prevent Atelectasis or to reopen collapsed lung tissue. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. On the average, arterial oxygenation does not improve markedly, and Atelectasis may persist. Further, reopened lung units re-collapse rapidly after discontinuation of PEEP. Inflation of the lungs to an airway pressure of 40 cm H_2O, maintained for 7–8 seconds (recruitment or “vital capacity” manoeuvre), re-expands all previously collapsed lung tissue. During induction of anaesthesia, the use of a gas mixture, that includes a poorly absorbed gas such as nitrogen, may prevent the early formation of Atelectasis. During ongoing anaesthesia, pulmonary collapse reappears slowly if a low fraction of oxygen in nitrogen is used for the ventilation of the lungs after a previous VC-manoeuvre. On the other hand, ventilation of the lungs with pure oxygen results in a rapid reappearance of Atelectasis. Thus, ventilation during anaesthesia should be done if possible with a moderate fraction of inspired oxygen (FIO_2, e.g. 0.3–0.4). Alternatively, if the lungs are ventilated with a high inspiratory fraction of oxygen, the use of PEEP may be considered. In summary, Atelectasis is present in most humans during anaesthesia and is a major cause of impaired oxygenation. Avoiding high fractions of oxygen in inspired gas during induction and maintenance of anaesthesia may prevent formation of Atelectasis. Finally, intermittent “vital capacity”-manoeuvres together with PEEP reduces the amount of Atelectasis and pulmonary shunt.
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Atelectasis and pulmonary shunting during induction of general anaesthesia--can they be avoided?
Acta Anaesthesiologica Scandinavica, 1996Co-Authors: Hans Ulrich Rothen, B. Sporre, Goran Engberg, G. Wegenius, A Reber, Goran HedenstiernaAbstract: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.
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re expansion of Atelectasis during general anaesthesia a computed tomography study
BJA: British Journal of Anaesthesia, 1993Co-Authors: Hans Ulrich Rothen, B. Sporre, Goran Engberg, G. Wegenius, Goran HedenstiernaAbstract: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.
J Milicemili - One of the best experts on this subject based on the ideXlab platform.
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the effect of lung expansion and positive end expiratory pressure on respiratory mechanics in anesthetized children
Anesthesia & Analgesia, 2008Co-Authors: Athanasios G Kaditis, Etsuro K Motoyama, Nobuhiro Maekawa, Isuta Nishio, Taiyo Imai, J MilicemiliAbstract:BACKGROUND:Imaging studies have shown that general anesthesia in children results in Atelectasis. Lung recruitment total lung capacity (TLC) maneuvers plus positive end-expiratory pressure (PEEP) are effective in preventing Atelectasis. However, physiological changes in children during general anest
Athanasios G Kaditis - One of the best experts on this subject based on the ideXlab platform.
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the effect of lung expansion and positive end expiratory pressure on respiratory mechanics in anesthetized children
Anesthesia & Analgesia, 2008Co-Authors: Athanasios G Kaditis, Etsuro K Motoyama, Nobuhiro Maekawa, Isuta Nishio, Taiyo Imai, J MilicemiliAbstract:BACKGROUND:Imaging studies have shown that general anesthesia in children results in Atelectasis. Lung recruitment total lung capacity (TLC) maneuvers plus positive end-expiratory pressure (PEEP) are effective in preventing Atelectasis. However, physiological changes in children during general anest
