Services on Demand
Print version ISSN 0034-7094
On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.58 no.1 Campinas Jan./Feb. 2008
Atelectasis during anesthesia: pathophysiology and treatment*
Atelectasias durante anestesia: fisiopatología y tratamiento
Luiz Marcelo Sá Malbouisson, TSAI; Flávio HumbertoII; Roseny dos Reis Rodrigues, TSAII; Maria José Carvalho Carmona, TSAIII; José Otávio Costa Auler Jr. TSAIV
em Ciências pela Universidade de São Paulo; Médico Supervisor
da Divisão de Anestesiologia do HCFMUSP; Coordenador da UTI da Disciplina
de Anestesiologia do Instituto Central do HCFMUSP; Especialista em Terapia Intensiva-AMIB
IIMédico Assistente do Serviço de Anestesiologia e Terapia Intensiva do Instituto do Coração (InCor) do HCFMUSP
IIIProfessora-Associada da Disciplina de Anestesiologia da FMUSP; Diretora da Divisão de Anestesiologia do Instituto Central do HCFMUSP
IVProfessor Titular da Disciplina de Anestesiologia da FMUSP; Diretor do Serviço de Anestesiologia e Terapia Intensiva Cirúrgica do Instituto do Coração (InCor) do HCFMUSP
METHODS: The incidence of intraoperative pulmonary collapse is elevated
in patients undergoing surgery under general anesthesia with muscle relaxation/paralysis.
This complication is associated with worsening intraoperative gas exchange and,
in some cases, the need for prolonged postoperative respiratory support. The
objective of this report was to review the pathophysiological aspects of atelectasis
during general anesthesia and possible therapeutic maneuvers that could prevent
and treat this complication.
CONTENTS: This review discusses the concepts about the incidence of intraoperative atelectasis, factors that influence their development, both mechanical and those related to mechanical ventilator settings during the surgery, diagnostic criteria, and strategies to prevent and treat this complication.
CONCLUSIONS: Understanding of the mechanisms related with the development of intraoperative pulmonary collapse, as well as its treatment, can contribute to reduce the incidence of postoperative pulmonary complications, the length of recovery and hospital costs.
Key Words: COMPLICATIONS: atelectasis, pulmonary collapse; VENTILATION: mechanical controlled, alveolar recruitment maneuver, positive end-expiratory pressure.
Y OBJETIVOS: El colapso pulmonar intraoperatorio es una complicación
de elevada incidencia en pacientes sometidos a la intervención quirúrgica
bajo anestesia general con relajamiento/parálisis de la musculatura.
Esta complicación está asociada al empeoramiento de los cambios
de gas en el intraoperatorio y en algunos casos, necesidad de soporte respiratorio
prolongado en el período postoperatorio. Los objetivos de este estudio
fueron los de revisar los aspectos fisiopatológicos de la formación
de atelectasias durante anestesia general y las posibles maniobras terapéuticas
para prevenir y tratar esa complicación.
CONTENIDO: En esta revisión, los conceptos sobre la incidencia de atelectasias intraoperatorias, los factores relacionados a su desarrollo, tanto mecánicos como los relacionados al ajuste del respirador durante el procedimiento quirúrgico, los aspectos del diagnóstico y las estrategias de prevención y tratamiento fueron abordados de manera sistemática.
CONCLUSIONES: La comprensión de los mecanismos relacionados al desarrollo del colapso pulmonar durante el período intraoperatorio, como también su tratamiento, pueden contribuir para la reducción de la incidencia de complicaciones pulmonares postoperatorias, el tiempo de recuperación y los costes de las internaciones en los hospitales.
Postoperative pulmonary complications after major surgeries have been described since the beginning of the XX Century, being treated with high concentrations of inspired oxygen 1-3. After the introduction of intraoperative mechanical ventilation in anesthesia, progressive reduction in elastic lung recoil and deterioration of blood oxygenation were noted during surgeries, even in patients with prior normal lung function 2-4. Bendixen et al. proposed that this progressive reduction of elastic lung recoil and arterial oxygenation were caused, mainly, by a collapse of air spaces and, partly, by changes in superficial pulmonary tension, introducing the concept of intraoperative atelectasis in clinical practice 5. That same year, Bergman reported for the first time a reduction in residual volume (RV) in patients undergoing general anesthesia and mechanical ventilation 6. This reduction in RV was attributed to pulmonary collapse and associated with changes in ventilation/perfusion ratio and hypoxemia during anesthesia 7,8. Bendixen et al. observed that consecutive pulmonary hyperinflation during anesthesia was capable to restore arterial oxygenation and lung recoil 5. Since then, several studies have evaluated the factors related with the development of intraoperative atelectasis and the use of alveolar recruitment maneuvers. In this report, we reviewed the incidence and mechanisms of intraoperative pulmonary collapse and alveolar recruitment maneuvers with emphasis on cardiothoracic surgeries.
DEFINITION AND INCIDENCE OF INTRAOPERATIVE ATELECTASIS
Intraoperative atelectasis is defined as pulmonary collapse that occurs after anesthetic induction being characterized, clinically, by a reduction in lung elastic recoil and compromised arterial oxygenation. It is estimated that the incidence of atelectasis during anesthesia varies between 50% and 90% of adult patients undergoing general anesthesia, both during spontaneous and mechanical ventilation 9,10. According to Moller et al., mild to moderate hypoxemia as a consequence of intraoperative pulmonary collapse, defined as hemoglobin saturation between 85% and 90%, affects approximately 50% of patients undergoing general anesthesia for elective surgeries despite the use of an inspired fraction of oxygen of 0.4 9. Using CT scan of the thorax, Lundquist et al. studied 109 patients scheduled for elective abdominal surgeries under general anesthesia. In this study, it was observed the presence of dependent pulmonary densities in 95 patients (87%), which were interpreted as representing atelectasis. Two different types of atelectasis were described, pulmonary densities distributed homogenously in 78% of the patients and in 9% they were not distributed homogeneously 10.
In patients undergoing cardiac procedures, the development of atelectasis is a frequent complication and difficult to reverse postoperatively. In our institution, mild to moderate hypoxemia in the immediate postoperative period was detected in 52% of 461 patients undergoing elective myocardial revascularization (MR), and, according to Magnusson et al. 11, atelectasis were the greatest cause of hypoxemia and shunting after cardiopulmonary bypass (CPB). A study by Gale et al. on the incidence of pulmonary complications after cardiac surgery with CPB found radiographic evidence of atelectasis in 64% of 50 patients operated consecutively 12. On the first postoperative day, Tenling et al. performed CT scans of the chest in 18 patients who underwent change of the mitral valve or MR with cardiopulmonary bypass. They observed bilateral dependent pulmonary densities in all but one patient. Those pulmonary densities corresponded approximately to 20% of collapsed lung parenchyma 13. A study by Vargas et al. on late pulmonary complications in 125 patients who underwent CPB observed that 30 patients had normal chest X-rays, 38 had atelectasis and 57 had pleural effusion six days after the surgery 14. The authors also observed a mean reduction in forced vital capacity (FVC) in 33.4% of the patients and in forced expiratory volume in 1 second (FEV1) in 33.5% of the patients with atelectasis. According to the same group, the most important reduction in FVC occurs immediately after the surgery, improving gradually. However, until the tenth postoperative day FVC remained more than 30% below preoperative values 15.
MECHANISMS OF INTRAOPERATIVE PULMONARY COLLAPSE
Several mechanisms are involved in intraoperative atelectasis formation and reduction in functional residual capacity (FRC), and they can be divided in three groups: mechanical compression of lung parenchyma, absorption of alveolar gases and surfactant dysfunction. Mechanically, the degree of pulmonary insufflation depends on the transpulmonary pressure, i.e., alveolar pressure minus pleural pressure. Physiologically, there is an increase in pleural pressure in dependent and caudal portions of the lungs, close to the diaphragm, with consequent antero-posterior and cephalad-caudal transpulmonary pressures gradient or pulmonary insufflation. Under physiological conditions, alveoli in the bases of the lungs are less insufflated than those in the apices. In patients breathing spontaneously, during inspiration the pleural pressure is more negative at the bases due to the contraction of the diaphragm, contributing for the maintenance of positive transpulmonary pressure and permeability of the small airways and alveoli in those regions. After induction of anesthesia, pleural pressure becomes positive due to muscular relaxation and intrathoracic dislocation of the relaxed diaphragm, weight of the heart on the pulmonary parenchyma and compression of dependent regions of the lung caused by the weight of the lung itself. When a patient with normal lungs is placed in ventral decubitus, the weight of the pulmonary parenchyma is transmitted to the pleura generating an increase in pressure of 0.25 g.cm-2 for each centimeter in the antero-posterior axis, while in patients with an acute inflammatory process and ARDS it increases by 1 g.cm-2 16,17. The transmission of the pressure imposed by the overlying lung parenchyma compresses the airways and alveoli, leading to pulmonary collapse. At the same time, the relaxation of the diaphragm after anesthetic induction causes it to be dislocated upwards, under the weight of the abdominal organs, compressing the lungs and increasing pleural pressure, with the consequent reduction in transpulmonary pressure in more dependent and caudal regions of the lungs 18,19. Even in awaken patients, the supine position is associated with a reduction in FRC of 0.5 to 1 L when compared with the orthostatic position 20. The elevation of the diaphragm secondary to anesthesia and muscle paralysis is associated with an additional reduction of 0.5 to 1 L in FRC in patients in dorsal decubitus 21-23. In obese patients undergoing upper abdominal surgery or laparoscopy, the elevation of the diaphragm can be even more pronounced, worsening pulmonary collapse in the dorsal areas of the lungs secondary to the weight of the abdominal adipose tissue 24. The direct compression of the inferior lobes by the heart and mediastinal structures is another factor that can contribute to reduce transpulmonary pressure in dependent and caudal regions of the lungs 25-27. In the supine position, the heart and other mediastinal structures rest on the medial regions of the inferior lobes, exerting a 5 cmH2O.cm-2 pressure in adult patients without cardiac diseases, and approximately 7 to 8 cmH2O.cm-2 in patients with acute pulmonary lesion 27.
In anesthetized patients on mechanical ventilation, the mechanical compression of dependent and caudal lung regions is probably the most important factor in the development of intraoperative pulmonary collapse 26,28,29. In a study by Brismar et al. of patients undergoing abdominal surgery under general anesthesia, CT scan of the chest demonstrated pulmonary densities that were more pronounced in caudal regions than in the upper areas of the lungs 30. Similar results were reported by Warner et al. in healthy volunteers undergoing general anesthesia with halothane 31, by Tenling et al. in patients undergoing cardiac surgeries 13, and Puybasset et al. in patients with postoperative acute pulmonary lesion 22,32,33.
The absorption of alveolar gas is also implicated in the development of intraoperative atelectasis, even in the absence of airways obstruction. The use of high inspired fractions of oxygen has also been reported as one of the causes of pulmonary collapse. Joyce and Williams postulated that after anesthetic induction the airways in the dependent areas of the lungs behave as a closed cavity, prone to collapse. Using a mathematical model, the authors proposed that prior oxygenation and the use of high inspired fraction of oxygen increased the capture of gas from poorly ventilated areas of the lungs, being the main factors responsible for atelectasis formation 34. Rothen et al., studying 12 patients undergoing elective surgery under general anesthesia, observed that when a FiO2 of 1 was used after maneuvers of pulmonary expansion up to the tidal volume (a 40 cmH2O pressure in the airways), atelectasis were evident in chest CT scans in up to five minutes. When patients were ventilated using an inspired oxygen fraction of 40% after pulmonary expansion, atelectasis were observed only after 40 minutes 35. Rothen et al. also reported an increase in pulmonary shunting from 0.3% to 2.1% in surgical patients with normal lungs undergoing general anesthesia, and a small proportion of atelectasis were detected in CT scans of the chest obtained after anesthetic induction when patients were ventilated with FiO2 of 0.3. Using FiO2 of 1, instead of 0.3, increased pulmonary shunting by 6.5% and atelectasis developed in a larger proportion of the pulmonary parenchyma 36. There have been reports in the literature associating high inspired fractions of oxygen and pulmonary collapse for at least fifty years 8. Although some benefits have been attributed to the use of high oxygen concentrations during anesthesia, such as reduction in postoperative nausea and vomiting 37, increase in pro-inflammatory responses and antimicrobiotic activity of alveolar macrophages 38, possible reduction in postoperative infection of the surgical wound 39 and prevention of episodes of hypoxemia, postoperative atelectasis do not reverse immediately and might persist for several days increasing the time of mechanical ventilation required, the need of respiratory therapy, increased length of hospitalization and health care costs. Weighing those data carefully, current evidence does not indicate that the possible benefits of the use of high oxygen concentrations can overcome the detrimental consequences of postoperative pulmonary complications.
Dysfunction of the surfactant system is a third factor related with the development of intraoperative atelectasis. The surfactant plays an important role in the prevention of alveolar collapse, reducing alveolar superficial tension and stabilizing alveolar structures 40. Evidence obtained from experimental studies of the analysis of pressure-volume curves of isolated dog lung demonstrated a reduction in maximal lung volume, which was proportional to the increase in inhalational anesthetic 41. In children undergoing cardiac surgery with cardiopulmonary bypass, Friedrich et al. observed marked changes in the composition in surfactant phospholipids and proteins after CPB 42. Those results were confirmed by Griese et al., who observed prolonged surfactant dysfunction after cardiac surgery with CPB 43. However, the role of the surfactant in the development of intraoperative atelectasis is controversial, since it has a turnover of 14 hours, which is enough for most surgeries.
Additionally, it is also important to consider the role of the anesthesiologist on the genesis of intraoperative pulmonary collapse. Atelectasis have been described in patients undergoing both intravenous and inhalational anesthesia or combined anesthesia 5,44. Regardless of the anesthetic technique used, adjustment of respiratory parameters after endotracheal intubation has an important role in the prevention of atelectasis, especially when protective ventilatory strategies are used, with low tidal volumes without positive end-expiratory pressure (PEEP) on proper levels, especially in patients undergoing upper abdominal surgeries. Certainly, the use of elevated tidal volumes (> 10 mL.kg-1) does not offer protection against pulmonary collapse and it can exacerbate pulmonary lesions associated with mechanical ventilation, and, therefore, should not be used in clinical practice 45,46. The lack of PEEP during mechanical ventilation of patients undergoing general anesthesia with high inspired fraction of oxygen, even when associated with large tidal volumes, is an important factor for the development of intraoperative pulmonary collapse 47.
In patients undergoing cardiac surgeries, the use of cardiopulmonary bypass, independently of the sternectomy and thoracic manipulation, is related with the development of intraoperative atelectasis. Aspiration of the airways to remove the air from the lungs is another factor that can induce the development of atelectasis. Lu et al., using CT scan of the chest to study the effects of aspiration of the airways and pulmonary parenchyma in animals on mechanical ventilation with FiO2 of 0.3, observed that endotracheal suctioning resulted in the development of pulmonary collapse, a mean reduction in bronchial diameter of 29%, reduction in arterial oxygen saturation from 95% to 87%, increased shunting from 19% to 31%, and increased airways resistance. According to the data of those authors, the increase in FiO2 would interact synergistically with the aspiration of the airways, resulting in worsening of atelectasis, despite the protection against transitory hypoxemia caused by suctioning 48.
CLINICAL CONSEQUENCES OF INTRAOPERATIVE ATELECTASIS IN PATIENT EVOLUTION
In a large proportion of patients undergoing general anesthesia and who returned to the general ward afterwards, after resuming spontaneous ventilation and early ambulation, most of intraoperative atelectasis show reversion within 24 hours, without any clinical or pulmonary compromise 24. However, patients undergoing major surgeries, especially cardiac surgeries and those involving the upper abdomen, develop large areas of atelectasis, which usually are responsible for an increase in hospital stay and the need of intensive respiratory treatment. As mentioned before, a reduction in FRC can persist for up to 10 days after cardiac surgeries. The presence of atelectasis predisposes the lungs to the harmful the effects associated with mechanical ventilation or worsens preexisting lung lesions. Some studies have demonstrated the presence of pulmonary lesion caused by the mechanical distension of normally inflated parenchyma. Since the tidal volume is distributed to the inflated pulmonary parenchyma, the tidal volume that will be distributed to non-collapsed regions of the lungs increases proportionally to the volume of collapsed lung, leading to sustained hyperinflation of those regions and possible volumetric trauma/barotrauma and inflammation, with their deleterious consequences to the lung tissue 45,49,50. The noxious effects of relatively increased tidal volume distributed to non-collapsed pulmonary parenchyma has been established in patients with acute lung lesions 51,52 and the same might be true for patients undergoing prolonged general anesthesia who develop collapse of certain areas of the lungs, therefore increasing the incidence of postoperative respiratory complications. Other repercussions of perioperative pulmonary complications associated with atelectasis include the need of intense respiratory therapy, prolonged stay in the ICU and an increase in the incidence of postoperative pneumonia 53.
CLINICAL EVALUATION OF INTRAOPERATIVE ATELECTASIS
Changes in arterial oxygenation and reduction in pulmonary elastic recoil are the first physiologic changes that suggest the presence of atelectasis after anesthetic induction. The pressure-volume curve of the respiratory system also provides some clues of the presence of atelectasis, such as an almost static reduction in elastic recoil and the development of a lower inflexion point. Conventional chest X-rays may demonstrate lines or opacification, deviation of interlobar fissures, and loss of volume of the affected segment or lobe. Deviation of the mediastinum or of the hemidiaphram and the reduction of the intercostal spaces are other radiological signs suggestive of atelectasis. Conventional chest X-rays cannot detect properly pulmonary collapse in small areas of the lungs or in areas with superposition of structures.
Despite being the standard exam to detect atelectasis, this exam cannot be done during the surgery and, therefore, the diagnosis of intraoperative pulmonary collapse is based on the reduction of elastic recoil and worsening gas exchange, which, once detected, mandate the institution of maneuvers to revert the atelectasis, besides the use of preventive measures.
ALVEOLAR RECRUITMENT MANEUVERS DURING SURGERY
Since the first reports of worsening arterial oxygenation and reduction in pulmonary elastic recoil in animal models under general anesthesia and mechanical ventilation using a "normal tidal volume" by Mead et al. and Ferris et al., pulmonary expansion maneuvers, like deep inspirations, have been described as capable of reversing the reduction in oxygenation and elastic recoil 54,55. Bendixen et al. observed that the reduction in pulmonary elastic recoil and arterial oxygenation in surgical patients under general anesthesia and controlled mechanical ventilation returned to normal values when the lungs were hyperinflated up to the total lung capacity. They described the recruitment maneuver performed with three sustained inspirations with the reinhalation anesthetic bag, with a pressure of 20 cmH2O for 10 seconds in the first insufflation, 30 cmH2O for 15 seconds on the second insufflation, and 40 cmH2O for 20 seconds5. One should note that opening of collapsed alveoli depends on elevated pressures and the time necessary to overcome the opening pressure.
Since the first reports of hyperinsufflation maneuvers to counteract the harmful effects of atelectasis on gas exchange and in respiratory mechanics, the use of recruitment maneuvers has become an important adjuvant of mechanical ventilation during general anesthesia. Other pulmonary recruitment protocols have been described by several authors to revert intraoperative pulmonary collapse. Among them, the use of three consecutive and sustained hyperinsufflations with an inspiratory pressure of 40 cmH2O for 30 seconds has demonstrated to be capable of re-expanding virtually all collapsed pulmonary areas in patients with normal lungs under general anesthesia for abdominal or cardiac surgeries 56,57. Another perioperative recruitment maneuver was described by Tusman et al., increasing PEEP up to 15 cmH2O and peak inspiratory pressure up to 40 cmH2O. Initially, the respiratory rate was adjusted to 8 breaths per minute with an inspiratory pause for 20% of the respiratory cycle. On a second step, the tidal volume was increased to 18 mL.kg-1 or the peak inspiratory pressure was limited to 40 cmH2O, and those parameters were maintained for at least 10 breaths. Positive end-expiratory pressure was increased progressively up to 15 cmH2O and maintained for 10 breaths. Afterwards, the tidal volume was decreased to baseline values by decrements of 5 cmH2O until achieving a level of PEEP that would prevent pulmonary collapse 48. This type of alveolar recruitment maneuver is interesting because ventilation is not interrupted, which could, in theory, prevent elevation of CO2 and avoid episodes of hypoxemia.
An important aspect related with the reopening of collapsed lung parenchyma after a recruitment maneuver is the prevention of relapse. The same factors predisposing the development of atelectasis will be present after the alveolar recruitment maneuver and will, most likely, be present until the end of anesthesia and the phase of anesthetic recovery, and the use of PEEP is necessary to prevent relapses in pulmonary collapse while patients remain intubated. The level of PEEP that should be used is still a question of debate. As described by Brismar et al., a PEEP of 10 cmH2O reduced the development of new pulmonary densities in patients ventilated with high oxygen concentrations after the recruitment maneuver as well as the need of further recruitment maneuvers 30. However, a fixed PEEP might not be enough or could have harmful hemodynamic effects without improving arterial oxygenation 59,60. The level of PEEP should be individualized and titrated according to the level of oxygenation, respiratory mechanics and hemodynamic response during the surgery. It should also be emphasized that, after recruitment maneuvers, the lower inspired oxygen fraction possible should be used to decrease the formation of atelectasis secondary to gas reabsorption.
Nonetheless, some questions concerning the intraoperative use of recruitment maneuvers in anesthetized patients, especially those undergoing cardiac surgery, have not been answered yet: 1) Which patient will benefit more from recruitment maneuvers? 2) Which protocol should be used for those maneuvers? 3) How many recruitment maneuvers should be performed during the surgery? 4) What is the adequate time interval between maneuvers? It is most likely that recruitment maneuvers would be well tolerated by most patients who develop progressive worsening of oxygenation during the surgery without short or long-term harmful effects. On the other hand, this maneuver might be harmful to patients with untreated marked right ventricular dysfunction, severe pulmonary hypertension, increased intracranial pressure, low cardiac output, or shock. Although frequently observed in clinical practice, one should never forget that pneumothorax, pneumomediastinum, and etc might occur after the implementation of recruitment maneuvers. Except for some contraindications, recruitment maneuvers, followed by the adequate use of PEEP, should be performed in any patient whose oxygenation worsens during surgery. Recruitment maneuvers can be repeated as often as necessary by the anesthesiologist. However, the need of successive recruitment maneuvers should indicate that the PEEP selected after prior recruitments maneuvers was not enough to prevent relapse of pulmonary collapse. Specific monitoring of intraoperative recruitment is based on functional pulmonary parameters, such as arterial oxygenation and pulmonary elastic recoil.
The probable benefits of alveolar recruitment maneuvers for atelectasis go beyond the mechanical and oxygenation effects. Homogenous distribution of ventilation after the opening of collapsed areas is associated with a reduction in pulmonary lesion caused by ventilation and reduced need of postoperative mechanical ventilation. Despite the lack of clear evidence linking the presence of atelectasis with postoperative pneumonia, the reduction of postoperative mechanical ventilation is associated with a reduced incidence of respiratory infections, reduced stay in the ICU and reduction in health care costs.
01. Pasteur W Active lobar collapse of the lung after abdominal operations. Lancet, 1910;2:1080-1083. [ Links ]
02. Nunn JF, Payne JP Hypoxaemia after general anaesthesia. Lancet, 1962;2:631-632. [ Links ]
03. Grigor KC Atelectasis during anaesthesia (spontaneous atelectasis). Anaesthesia, 1954;9:185-189. [ Links ]
04. Tibbs DJ Hypoxaemia after anaesthesia. Lancet 1965;14:1105-1106. [ Links ]
05. Bendixen HH, Hedley-Whyte J, Laver MB Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. A concept of atelectasis. N Engl J Med, 1963;269:991-996. [ Links ]
06. Bergman NA Distribution of inspired gas during anesthesia and artificial ventilation. J Appl Physiol 1963;18:1085-1089. [ Links ]
07. Bendixen HH Atelectasis and shunting. Anesthesiology, 1964;25:595-596. [ Links ]
08. Dery R, Pelletier J, Jacques A et al. Alveolar collapse induced by denitrogenation. Can Anaesth Soc J, 1965;12:531-557. [ Links ]
09. Moller JT, Johannessen NW, Berg H et al. Hypoxaemia during anaesthesiaan observer study. Br J Anaesth, 1991;66:437-444. [ Links ]
10. Lundquist H, Hedenstierna G, Strandberg A et al. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol, 1995;36:626-632. [ Links ]
11. Magnusson L, Zemgulis V, Wicky S et al. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology, 1997;87:1153-1163. [ Links ]
12. Gale GD, Teasdale SJ, Sanders DE et al. Pulmonary atelectasis and other respiratory complications after cardiopulmonary bypass and investigation of aetiological factors. Can Anaesth Soc J, 1979;26:15-21. [ Links ]
13. Tenling A, Hachenberg T, Tyden H et al. Atelectasis and gas exchange after cardiac surgery. Anesthesiology, 1998;89:371-378. [ Links ]
14. Vargas FS, Cukier A, Terra-Filho M et al. Influence of atelectasis on pulmonary function after coronary artery bypass grafting. Chest, 1993;104:434-437. [ Links ]
15. Vargas FS, Terra-Filho M, Hueb W et al. Pulmonary function after coronary artery bypass surgery. Respir Med, 1997;91:629-633. [ Links ]
16. Pelosi P, D'Andrea L, Vitale G et al. Vertical gradient of regional lung inflation in adult respiratory distress syndrome. Am J Respir Crit Care Med, 1994;149:8-13. [ Links ]
17. Tomiyama N, Takeuchi N, Imanaka H et al. Mechanism of gravity-dependent atelectasis. Analysis by nonradioactive xenon-enhanced dynamic computed tomography. Invest Radiol, 1993; 28:633-638. [ Links ]
18. Agostini E, D'Angelo E, Bonanni MV The effect of the abdomen on the vertical gradient of pleural surface pressure. Respiration Physiol, 1970;8:332-346. [ Links ]
19. Agostini E, D'angelo E, Bonanni MV Topography of pleural surface pressure above resting volume in relaxed animals. J Appl Physiol, 1970;29:297-306. [ Links ]
20. Nunn JF Respiratory Aspects of Anaesthesia, em: Nunn JF Applied Respiratory Physiology, 3th Ed, London, Butterworths, 1987;350-370. [ Links ]
21. Froese AB, Bryan AC Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology, 1974;41: 242-255. [ Links ]
22. Puybasset L, Cluzel P, Chao N et al. A computed tomography scan assessment of regional lung volume in acute lung injury. Am J Respir Crit Care Med, 1998;158:1644-1655. [ Links ]
23. Reber A, Nylund U, Hedenstierna G Position and shape of the diaphragm: implications for atelectasis formation. Anaesthesia, 1998;53:1054-1061. [ Links ]
24. Eichenberger A, Proietti S, Wicky S et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg, 2002;95:1788-1792. [ Links ]
25. Hoffman EA Effect of body orientation on regional lung expansion: a computed tomographic approach. J Appl Physiol, 1985; 59:468-480. [ Links ]
26. Hyatt RE, Bar-Yishay E, Abel MD Influence of the heart on the vertical gradient of transpulmonary pressure in dogs. J Appl Physiol, 1985;58:52-57. [ Links ]
27. Malbouisson LM, Busch CJ, Puybasset L et al. Role of the heart in the loss of aeration characterizing lower lobes in acute respiratory distress syndrome. Am J Respir Crit Care Med, 2000; 161:2005-2012. [ Links ]
28. Strandberg A, Hedenstierna G, Tokics L et al. Densities in dependent lung regions during anaesthesia: atelectasis or fluid accumulation? Acta Anaesthesiol Scand, 1986;30:256-259. [ Links ]
29. Yang QH, Kaplowitz MR, Lai-Fook SJ Regional variations in lung expansion in rabbits: prone vs. supine positions. J Appl Physiol, 1989;67:1371-1376. [ Links ]
30. Brismar B, Hedenstierna G, Lundquist H et al. Pulmonary densities during anesthesia with muscular relaxation a proposal of atelectasis. Anesthesiology, 1985;62:422-428. [ Links ]
31. Warner DO, Warner MA, Ritman EL Atelectasis and chest wall shape during halothane anesthesia. Anesthesiology, 1996;85: 49-59. [ Links ]
32. Puybasset L, Cluzel P, Chaw N et al. Distribution of volume reduction in post operative acute lung injury- factors influencing peep-induced alveolar recruitment. Br J Anaesth, 1997;78(suppl 1):A380. [ Links ]
33. Puybasset L, Cluzel P, Gusman P et al. Regional distribution of gas and tissue in acute respiratory distress syndrome. I. Consequences for lung morphology. Intensive Care Med, 2000;26: 857-869. [ Links ]
34. Joyce CJ, Williams AB Kinetics of absorption atelectasis during anesthesia: a mathematical model. J Appl Physiol, 1999; 86:1116-1125. [ Links ]
35. Rothen HU, Sporre B, Engberg G et al. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand, 1995;39:118-125. [ Links ]
36. 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;40:524-529. [ Links ]
37. Goll V, Akca O, Greif R et al. Ondansetron is no more effective than supplemental intraoperative oxygen for prevention of postoperative nausea and vomiting. Anesth Analg, 2001;92:112-117. [ Links ]
38. Kotani N, Hashimoto H, Sessler DI et al. Supplemental intraoperative oxygen augments antimicrobial and proinflammatory responses of alveolar macrophages. Anesthesiology, 2000;93: 15-25. [ Links ]
39. Greif R, Akca O, Horn EP et al. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med, 2000;342:161-167. [ Links ]
40. Nunn JF Applied Respiratory Physiology, 3th, London, Butterworths, 1987. [ Links ]
41. Woo SW, Berlin D, Hedley-Whyte J Surfactant function and anesthetic agents. J Appl Physiol, 1969;26:571-577 [ Links ]
42. Friedrich B, Schmidt R, Reiss I et al. Changes in biochemical and biophysical surfactant properties with cardiopulmonary bypass in children. Crit Care Med, 2003;31:284-290. [ Links ]
43. Griese M, Wilnhammer C, Jansen S et al. Cardiopulmonary bypass reduces pulmonary surfactant activity in infants. J Thorac Cardiovasc Surg, 1999;118:237-244. [ Links ]
44. Bendixen HH, Bullwinkel B, Hedley-Whyte J et al. Atelectasis and shunting during spontaneous ventilation in anesthetized patients. Anesthesiology, 1964;25:297-301. [ Links ]
45. Dreyfuss D, Basset G, Soler P et al. Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Resp Dis, 1985;132:880-884. [ Links ]
46. Dreyfuss D, Saumon G Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation. Am Rev Respir Dis, 1993;148: 1194-1203. [ Links ]
47. 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. [ Links ]
48. Lu Q, Capderou A, Cluzel P et al. A computed tomographic scan assessment of endotracheal suctioning-induced bronchoconstriction in ventilated sheep. Am J Respir Crit Care Med, 2000; 162:1898-1904. [ Links ]
49. Dreyfuss D, Saumon G Synergistic interaction between alveolar floading and distention during mechanical ventilation. Am J Respir Crit Care Med, 1996;153:A12. [ Links ]
50. Dreyfuss D, Soler P, Saumon G Mechanical ventilation-induced pulmonary edema. Interaction with previous lung alterations. Am J Resp Crit Care Med, 1995;151:1568-1575. [ Links ]
51. Gattinoni L, Pelosi P, Pesenti A et al. CT scan in ARDS: clinical and physiopathological insights. Acta Anaesthesiol Scand, 1991;(suppl 95):87-96. [ Links ]
52. Gattinoni L, Pesenti A The concept of "baby lung". Intensive Care Med, 2005;31:776-784. [ Links ]
53. Brooks-Brunn JA Postoperative atelectasis and pneumonia. Heart Lung, 1995;24:94-115. [ Links ]
54. Mead J, Collier C Relation of volume history of lungs to respiratory mechanics in anesthetized dogs. J Appl Physiol, 1959; 14:669-678. [ Links ]
55. Ferris BG Jr, Pollard DS Effect of deep and quiet breathing on pulmonary compliance in man. J Clin Invest, 1960;39:143-149. [ Links ]
56. Rothen HU, Sporre B, Engberg G et al. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth, 1993;71:788-795. [ Links ]
57. Magnusson L, Zemgulis V, Tenling A et al. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study. Anesthesiology, 1998;88:134-142. [ Links ]
58. Tusman G, Bohm SH, Tempra A et al. Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology, 2003;98:14-22. [ Links ]
59. Pelosi P, Caironi P, Bottino N et al. Positive end expiratory pressure in anesthesia. Minerva Anestesiol, 2000;66:297-306. [ Links ]
60. 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, 1999;91:1221-1231. [ Links ]
Dr. Luiz Marcelo Sá Malbouisson
Av. Dr. Enéas de Carvalho Aguiar, 44, 2° andar, Bloco I Cerqueira César
05403-900 São Paulo, SP
Submitted em 16
de outubro de 2006
Accepted para publicação em 23 de outubro de 2007
* Received from Disciplina de Anestesiologia do Instituto Central do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP), São Paulo, SP