Atelectasis occurs in the dependent parts of the lungs of most patients who are anesthetized. Development of atelectasis is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance, and development of lung injury. The adverse effects of atelectasis persist into the postoperative period and can impact patient recovery. This review article focuses on the causes, nature, and diagnosis of atelectasis. The authors discuss the effects and implications of atelectasis in the perioperative period and illustrate how preventive measures may impact outcome. In addition, they examine the impact of atelectasis and its prevention in acute lung injury.

IT has been known for decades that in patients with previously normal lungs, general anesthesia is associated with impaired oxygenation.1Pulmonary atelectasis was suspected as the major cause, based on the observation of a successive decrease in lung compliance and the partial pressure of arterial oxygen (Pao2), both of which returned toward normal after deep inflations of the lung.2Bendixen et al.  2thus demonstrated their concept of a progressive alveolar collapse during general anesthesia with mechanical ventilation. It is now known that atelectasis occurs in the most dependent parts of the lung of 90% of patients who are anesthetized and plays an important role in gas exchange abnormalities and reduced static compliance associated with acute lung injury (ALI).3This article reviews the causes, nature, and consequences of atelectasis, focusing on the role of atelectasis in development of perioperative morbidity, and illustrates how preventive measures could impact perioperative health. In addition, we discuss the impact of atelectasis and of its prevention in ALI.

Three sets of mechanisms have been proposed that may cause or contribute to the development of atelectasis,4including compression of lung tissue, absorption of alveolar air, and impairment of surfactant function. This section describes these three underlying “physiologic” causes of atelectasis; clinical factors that can modulate the development of atelectasis are described in a subsequent section.

Compression Atelectasis

Compression atelectasis occurs when the transmural pressure distending the alveolus is reduced to a level that allows the alveolus to collapse. The diaphragm normally separates the intrathoracic and abdominal cavities and, when stimulated, permits differential pressures in the abdomen and chest. After induction of anesthesia, the diaphragm is relaxed and displaced cephalad and is therefore less effective in maintaining distinct pressures in the two cavities. Specifically, the pleural pressure increases to the greatest extent in the dependent lung regions (fig. 1) and can compress the adjacent lung tissue. This is termed compression atelectasis .5 

Fig. 1. (  A and  B ) In normal lungs (  A ), the alveolar inflation and vascular perfusion are associated with low stress and are not injurious. Two separate barriers form the alveolar–capillary barrier, the microvascular endothelium, and the alveolar epithelium. In contrast, with atelectasis (  B ), alveolar inflation and deflation may be heterogeneous, and the resulting airway stress causes epithelial injury. Because the blood vessels are compressed, perfusion may be traumatic because of flow-induced disruption of the microvascular endothelium. Both epithelial and endothelial injury may initiate or propagate lung injury. This figure depicts the advanced stage of lung injury caused by atelectasis. The initial injury is simple collapse of alveoli. However, with time, this leads to an inflammatory reaction. As the derecruited lungs cause epithelial injury and loss of epithelial integrity, both type I and type II alveolar cells are damaged. Injury to type II cells disrupts normal epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. In addition to collapse, derecruited lungs also become fluid filled. Neutrophils adhere to the injured capillary endothelium and migrate through the interstitium into the alveolar airspace. In the airspace, alveolar macrophages secrete cytokines, interleukin (IL)-1, -6, -8, and -10, and tumor necrosis factor (TNF)-α, which act locally to stimulate chemotaxis and activate neutrophils. IL-1 can also stimulate the production of extracellular matrix by fibroblasts. Neutrophils can release oxidants, proteases, leukotrienes, and other proinflammatory molecules, such as platelet-activating factor (PAF). MIF = macrophage inhibitory factor. 

Fig. 1. (  A and  B ) In normal lungs (  A ), the alveolar inflation and vascular perfusion are associated with low stress and are not injurious. Two separate barriers form the alveolar–capillary barrier, the microvascular endothelium, and the alveolar epithelium. In contrast, with atelectasis (  B ), alveolar inflation and deflation may be heterogeneous, and the resulting airway stress causes epithelial injury. Because the blood vessels are compressed, perfusion may be traumatic because of flow-induced disruption of the microvascular endothelium. Both epithelial and endothelial injury may initiate or propagate lung injury. This figure depicts the advanced stage of lung injury caused by atelectasis. The initial injury is simple collapse of alveoli. However, with time, this leads to an inflammatory reaction. As the derecruited lungs cause epithelial injury and loss of epithelial integrity, both type I and type II alveolar cells are damaged. Injury to type II cells disrupts normal epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. In addition to collapse, derecruited lungs also become fluid filled. Neutrophils adhere to the injured capillary endothelium and migrate through the interstitium into the alveolar airspace. In the airspace, alveolar macrophages secrete cytokines, interleukin (IL)-1, -6, -8, and -10, and tumor necrosis factor (TNF)-α, which act locally to stimulate chemotaxis and activate neutrophils. IL-1 can also stimulate the production of extracellular matrix by fibroblasts. Neutrophils can release oxidants, proteases, leukotrienes, and other proinflammatory molecules, such as platelet-activating factor (PAF). MIF = macrophage inhibitory factor. 

Close modal

Several lines of evidence support a role of the diaphragm in this setting. Froese and Bryan6used cineradiography to demonstrate a cephalad shift of the diaphragm during anesthesia and spontaneous breathing, which did not progress after muscle relaxation. However, a difference in the pattern of diaphragmatic movement was noted. In supine patients, during spontaneous breathing, the lower, dependent portion of the diaphragm moved the most, whereas with muscle paralysis, the upper, nondependent part showed the largest displacement. Two distinctly different patterns of diaphragmatic displacement were seen from the same new functional residual capacity (FRC) position. In an anesthetized patient breathing spontaneously, the active tension in the diaphragm is capable of overcoming the weight of the abdominal contents, and the diaphragm moves the most in the lower, dependent portion (because the lower or posterior diaphragm is stretched higher into the chest, it has the smallest radius of curvature and therefore contracts most effectively). In addition, the diaphragm is thicker posteriorly than anteriorly, and this may account for the disproportionate movement.7During paralysis and positive-pressure ventilation, the passive diaphragm is displaced by the positive pressure preferentially in the upper, nondependent portion (where there is least impedance to diaphragmatic movement). Subsequent studies confirmed these findings and, in addition, documented a reduction in the transverse area of the chest.8Using an advanced computed tomography (CT) scanner, Krayer et al.  9demonstrated a reduced thoracic cross-sectional area in anesthetized subjects but had more variable results regarding shape and position of the diaphragm; some subjects showed a cranial shift of the diaphragm, but in other subjects, part of the diaphragm was unaffected or even moved caudally. Other investigators have also shown results inconsistent with the classic model of regional ventilation10; nevertheless, it can be concluded that FRC is reduced in the anesthetized subject, whether caused by loss of traction of the chest wall or compression of the lung. Loss of intercostal muscle function may also contribute to reduced FRC during anesthesia. Inhalation agents decrease intercostal muscle activity, particularly in children.11 

Hedenstierna et al.  8also noted an additional source of lung compression in that there was a net shift of central blood volume from the thorax, which seemed to pool in the abdomen, resulting in additional dependent pressure arising from the abdomen and acting on the diaphragm. Finally, the displacement of the diaphragm has been studied under dynamic conditions, whereby increases in diaphragm tension through phrenic nerve stimulation have been shown to reduce the amount of atelectasis at isovolumic conditions in anesthetized patients.12 

Therefore, compression atelectasis occurs during general anesthesia and is caused by chest geometry, overall cephalad diaphragm displacement, differential regional diaphragmatic changes, shift of thoracic central vascular blood into the abdomen, and altered diaphragmatic dynamics.

Gas Resorption

Resorption atelectasis—sometimes called gas atelectasis  4—can occur by two mechanisms. After complete airway occlusion, a pocket of trapped gas is created in the lung unit distal to the obstruction. Because gas uptake by the blood continues and gas inflow is prevented by blocked airways, the gas pocket collapses.13Under these conditions, the rate of absorption of gas from an unventilated lung area increases with elevation of the fraction of inspired oxygen (Fio2).14 

A somewhat different mechanism explains absorption atelectasis in the absence of airway occlusion. In this context, lung zones that have low ventilation relative to perfusion (low ventilation/perfusion [VA/Q] ratio) have a low partial pressure of alveolar oxygen (Pao2) when air is breathed. When the Fio2is increased, Pao2increases, causing the rate at which oxygen moves from the alveolar gas to the capillary blood to increase greatly. The oxygen flux may increase so much that the net flow of gas into the blood exceeds the inspired flow of gas, and the lung unit becomes progressively smaller. Collapse is most likely to occur when the Fio2(and duration of exposure) is high or where the VA/Q ratio (and mixed venous oxygen content) is low.15,16 

Surfactant Impairment

Pulmonary surfactant that covers the large alveolar surface is composed of phospholipids (mostly phosphatidylcholine), neutral lipids, and surfactant-specific apoproteins (termed surfactant proteins A , B , C , and D ). By reducing alveolar surface tension, pulmonary surfactant stabilizes the alveoli and prevents alveolar collapse. This stabilizing function of surfactant may be depressed by anesthesia, and such an effect has been confirmed in vitro  by Woo et al.  17The authors evaluated the effect of anesthetic agents on surfactant function using deflation pressure–volume curves in excised dog lungs. They found that the reduction in percent maximum lung volume was proportional to the concentration of both chloroform and halothane.17Wollmer et al.  18also used pulmonary clearance of technetium-labeled diethylenetriamine pentaacetic acid to demonstrate that halothane anesthesia, in combination with high oxygen concentration, caused increased permeability of the alveolar–capillary barrier in rabbit lungs. The authors postulated that the increased rate of pulmonary clearance of technetium-labeled diethylenetriamine pentaacetic acid during anesthesia with halothane was likely to be caused by combined effects on the pulmonary surfactant or the alveolar epithelium or both.18In addition, it is known that the content of alveolar surfactant in isolated lungs is modified by mechanical factors. Hyperventilation by increased tidal volume,19sequential air inflations to total lung capacity,20or even a single cycle of increased tidal volume19all cause release of surfactant in isolated animal lungs. In rabbits, maintained increases in tidal volume increased the amount of total phospholipids recovered from bronchoalveolar lavages.21,22Supporting this is the report that the spontaneous occurrence of large gasping respirations increases the proportion of active forms of alveolar surfactant (phospholipids). Oyarzun et al.  23examined the ventilatory variables of cats breathing spontaneously during anesthesia for 4 h. They found that the frequency of large gasps is directly correlated with the concentration of phospholipids in bronchoalveolar lavage fluid.23 

All three mechanisms—compression, gas resorption, and surfactant impairment—may contribute to atelectasis formation during general anesthesia (fig. 2). However, given the surfactant reserve and the 14-h surfactant turnover time, it may be that primary changes in surface forces are less important; it is not known whether a collapsed alveolus can denature surfactant, and so the 14-h turnover time may not be relevant. Nonetheless, absorption and compression are considered to be the two mechanisms most implicated in perioperative atelectasis formation.24 

Fig. 2. This schematic outlines the probable pathogenic mechanisms underlying the development of atelectasis. Fio2= fraction of inspired oxygen; IV = intravenous; VA/Q = ventilation/perfusion ratio. 

Fig. 2. This schematic outlines the probable pathogenic mechanisms underlying the development of atelectasis. Fio2= fraction of inspired oxygen; IV = intravenous; VA/Q = ventilation/perfusion ratio. 

Close modal

Nature of Atelectasis

The following section reviews the characteristics of atelectasis in several clinical contexts and then reviews contemporary concepts regarding the nature of atelectasis.

Atelectasis due to Anesthesia.

Anesthesia-induced atelectasis is traditionally thought of as collapse of alveoli. Brismar et al.  5showed that within 5 min after induction of anesthesia, areas of increased density appeared in the dependent regions of both lungs on CT. The dense areas had an attenuation factor that corresponds to blood and connective tissue and indicates the absence of air. Injection of radiocontrast in the pleural space showed that the densities were located above the pleura, i.e. , within the lung.25Hedenstierna et al.  26also found these densities in anesthetized sheep and confirmed histologically that the densities were collapsed lung regions and not fluid accumulation.

Methods to restore normal FRC and various reexpansion maneuvers have been suggested. The application of positive end-expiratory pressure (PEEP) has been tested in several studies. Arterial oxygenation does not usually improve markedly, and atelectasis may persist.27,28Reopened units recollapse rapidly after discontinuation of PEEP. However, Rothen et al.  29,30demonstrated in volunteers that peak inspiratory pressures of at least 40 cm H2O were needed to fully reverse anesthesia-induced collapse of healthy lungs, and most of the reexpanded atelectatic lung tissue remains inflated for at least 40 min.

Direct Visualization of Atelectasis.

Using a unique in vivo  microscopic technique, Halter et al.  31viewed alveoli in the living animal in real time during mechanical ventilation. In a surfactant deactivation model of acute respiratory distress syndrome (ARDS), they measured alveolar number and stability before, during, and after a recruitment maneuver with ventilation with either decreased or increased PEEP. They demonstrated that a recruitment maneuver opens atelectatic alveoli and that without adequate PEEP, alveoli are unstable and susceptible to derecruitment. Although associated with sampling limitations,32this elegant study was the first to directly demonstrate visual evidence of collapse of individual alveoli reflecting atelectasis and stabilization reflecting recruitment.32 

Cyclic Lung Recruitment.

Mechanical ventilation of areas of lung that are atelectatic is associated with repetitive collapse and reexpansion with each breath, often called cyclic recruitment . A conventional view of the effects of atelectasis on gas exchange conveys an image of mixed venous blood perfusing nonventilated or collapsed alveoli, resulting in a consistent and stable proportion of the pulmonary venous return that derives from deoxygenated blood.33This notional contribution (i.e. , deoxygenated blood added to oxygenated blood) is seen as the sum of two constant flow rates, resulting in a shunt fraction (Qs/Qt%)7that can be mathematically calculated.

However, we now know that the oxygen content of pulmonary venous blood varies significantly throughout the respiratory cycle as the shunt fraction changes with every breath. Baumgardner et al.  34tested the hypothesis that cyclic collapse of alveoli in dependent lung regions with every breath should lead to large oscillations in Pao2as shunt varies with the respiratory cycle. They placed a partial pressure of oxygen (Po2) probe in the brachiocephalic artery of rabbits after saline lavage. They found a significant effect of respiratory rate on the magnitude of oscillations; as the respiratory rate increased, the amplitude of oscillations became progressively smaller.32The higher respiratory rate avoided cyclic recruitment; i.e. , the shorter expiratory time allowed expiration without collapse. In practice, the beneficial effect of higher respiratory rates leading to improved oxygenation can be seen when ventilating pediatric patients and in particular neonates. This suggests that the dynamics of mechanical events leading to recruitment and derecruitment are important determinants of the amount of lung that is cyclically recruited.34A previous study by Williams et al.  35also showed within-breath arterial Po2oscillations in an animal model of ARDS and confirmed that Pao2oscillations occur in the atelectatic lung. The authors investigated the effect of PEEP on Pao2oscillations. They found that as PEEP was increased, the amplitude of the Pao2oscillation decreased and the mean Pao2increased.35Several studies have evaluated the effects of various inspiratory-to-expiratory ratios on gas exchange, lung mechanics, and FRC; the inspiratory-to-expiratory ratio per se  was not found to be a significant factor.36–38 

Atelectasis: Volume Loss versus  Fluid Filling.

More recently, it has been argued that the dependent injured lung is derecruited, not because it is collapsed but because it is filled with fluid.39Work by Gattinoni et al.  40–42had concluded that dependent portions of the injured lung are exposed to a compressive pressure from the increased weight of edematous lung and are collapsed. Such a “weight-of-the-lung” hypothesis has been studied, and it seems that the weight of the lung accounts for only approximately 20% of the vertical gradient in pleural pressure and alveolar volume in normal lungs.43–45Hubmayr39suggests an alternative view of the mechanics of injured lungs based on lung weight, shape matching, interpretation of CT images of the lung, and pressure–volume curves. For example, where edema fluid and foam fill dependent regions, high inflation pressures are required to inflate with air, as opposed to low pressures required for inflation with fluid. The pressure–volume characteristics of the former more closely display the classic findings associated with atelectasis, including the prominent “lower inflection point” reflecting opening pressure.39Evidence in support of edema as the source of regional impedance in ARDS include parenchymal marker studies in oleic acid–injured lungs.46The parenchymal marker technique describes the topographic distribution of regional volume and ventilation in laboratory animals. The authors found that oleic acid injury did not produce collapse of dependent lung units in this model of ARDS.46They proposed an alternative mechanism for the topographic variability in regional impedances and lung expansion after injury, which was liquid or foam in alveoli and conducting airways.46 

Factors Modulating the Formation of Atelectasis

It is important for clinicians to understand how atelectasis develops or worsens in the clinical context. Several important clinical events act as modifiers that influence the formation of atelectasis (fig. 2).

Type of Anesthesia.

Atelectasis develops with both intravenous and inhalational anesthesia, regardless of whether the patient is breathing spontaneously or is paralyzed and mechanically ventilated.47–49Ketamine is the only anesthetic that does not produce atelectasis when used alone, although in conjunction with neuromuscular blockade, it does result in atelectasis.50 

Ventilatory effects of regional anesthesia depend on the type and extension of motor blockade.4Neuroaxial blockade that has significant cephalad extension reduces inspiratory capacity by up to 20%, and expiratory reserve volume approaches zero51; less extensive blockade affects pulmonary gas exchange only minimally, and arterial oxygenation and carbon dioxide elimination are well maintained during most spinal and epidural anesthesia.52,53Closing capacity and FRC remain unchanged.54 

Impact of Time.

The maximum decrease in FRC seems to occur within the first few minutes of general anesthesia.5,55During anesthesia for surgical operations on the limb, FRC is not influenced further by depth or duration of anesthesia.55,56Don et al.  55studied patients undergoing peripheral limb surgery who were free of cardiac and respiratory disease. Patients were divided into two groups, those breathing halothane in 100% oxygen and those breathing halothane in 30% oxygen in nitrogen. The FRC decreased comparably in both groups after induction of anesthesia, but this did not progress with time. However, other studies have found that during abdominal or thoracic surgery, pulmonary gas exchange deteriorates progressively during the course of the operation57,58; these studies were unable to determine the independent impact of time on atelectasis as opposed to surgical manipulation (e.g. , surgical packing, tissue retraction).

Effects of Position.

In adults, changing from the upright to the supine position results in a decrease of 0.5 l in FRC to 1.0 l, even in the awake state.7After anesthesia, FRC is reduced by a further 0.5 l to 0.7 l.49The Trendelenburg position allows the abdominal contents to push the diaphragm further cephalad, resulting in a further decrease in FRC.59In the lateral decubitus position, the dependent lung is predisposed to atelectasis, whereas the nondependent lung may have an increased FRC. The overall result is usually a slight increase in total lung FRC, which, despite the differences in lung size, is independent of whether the right or the left lung is in the dependent position.60The prone position may increase FRC slightly,61although this may not decrease atelectasis. In fact, distribution of ventilation is more uniform in anesthetized patients in the prone position, in particular where the abdomen is not supported.62Prone positioning improves oxygenation in patients with ARDS.63Animal models have also demonstrated the benefit of prone positioning after oleic acid–induced lung injury as well as a model of lung injury induced solely by mechanical forces.64,65Prone positioning causes less extensive histologic injury and alters its distribution.64,65 

Atelectasis is more prominent after cardiac surgery with cardiopulmonary bypass (CPB) than after other forms of surgery. Using a porcine model, Magnusson et al.  66found that atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy. Furthermore, the CPB-associated atelectasis accounted for most of the marked post-CPB increase in shunt and hypoxemia.66Clinical experience is consistent with laboratory reports, and prominent atelectasis has been noted in the dorsal lung regions on the first postoperative day in cardiac surgery patients.67Other causes of gas exchange impairment after sternotomy and CPB have been investigated, including pulmonary endothelial permeability.68Macnaughton et al.  68did not find any increase in pulmonary endothelial permeability, and they hypothesized that the major component of the deterioration in lung function was probably atelectasis occurring during bypass. Numerous studies have shown that a lung recruitment strategy and PEEP improves oxygenation in patients after CPB.69,70In addition, the application of PEEP of 10 cm H2O during CPB to maintain lung inflation has been shown to be beneficial.71Many anesthetists intentionally inflate the patient’s lungs before coming off CPB and directly visualize equal expansion of the lungs. This simple maneuver may detect significant obstruction from secretions or blood in the endotracheal tube.

Inspired Oxygen.

High oxygen concentration has been associated with atelectasis formation, and this is important because use of high Fio2(i.e. , approaching 1.0) represents standard practice among many anesthesiologists.72Previous studies suggested that inspired oxygen concentration may not be an important independent predictor of anesthesia-associated atelectasis.5,55However, one of these studies used the helium-dilution technique to measure FRC, which may not be as sensitive as the CT that was used in later studies.55,73In the absence of preoxygenation, atelectasis is not seen directly after induction of anesthesia; however, when Fio2is increased to 1.0 before intubation, development of atelectasis is a consistent finding.74,75Concerns about oxygen-induced atelectasis are not restricted to induction of anesthesia; increasing Fio2at the end of surgery to 1.0 before extubation also causes additional atelectasis, which persists into the postoperative period.76However, the use of lower Fio2may increase the risk of hypoxemia, should airway management subsequently prove difficult and ventilation be threatened.77One study investigated how different oxygen concentrations may affect the formation of atelectasis and the decrease in arterial oxygen saturation during apnea.78The authors found that during routine induction of general anesthesia, 80% oxygen caused minimal atelectasis, but the time margin before desaturation occurred was significantly shortened compared with that of 100% oxygen.78In addition, evidence suggests that administration of supplemental oxygen reduces the incidence of wound infection and could be beneficial during anesthesia and recovery.79,80Another possible benefit of supplemental oxygen during anesthesia includes a reduced incidence of postoperative nausea and vomiting after colorectal surgery,81although this was not found in patients undergoing gynecologic laparoscopy.82 

The effects of nitrous oxide on lung volumes during anesthesia have also been studied.83–85There was no difference in the incidence of postoperative atelectasis if nitrous oxide in oxygen was used or if air in oxygen was used as the inspired gas.

In treating patients for induction of general anesthesia, anesthesiologists must trade off the very rare possibility of acute hypoxemia in the event of difficulty with airway management versus  the common and predictable—but generally mild—impact of hyperoxia-induced atelectasis on later intraoperative gas exchange. Therefore, the use of a lower Fio2to replace preoxygenation has not been recommended as a new standard in clinical practice.78 

Effects of Age.

In adulthood, progressive age is not associated with increased propensity for development of atelectasis.86However, in young children (aged 1–3 yr) atelectasis seems to develop more readily than in adults,87possibly because of the far greater thoracic wall compliance resulting in less outwardly directed lung distension forces.88In infants, contraction of the diaphragm may cause paradoxical inward movement of the highly deformable chest wall, resulting in loss of lung traction. The resultant atelectasis could reduce ventilatory efficiency, increase diaphragmatic fatigue, and thereby further increase the tendency for atelectasis development. In addition, type I and II muscle fibers are not fully developed in children who are younger than 2 yr. This makes them prone to respiratory failure and fatigue when there is extra stress put on their respiratory system, not only during general anesthesia89but also in the presence of a respiratory tract infection, epiglottitis, or airway obstruction.

Closing volume is also greater in young children in whom the elastic supporting structure of the lung is incompletely developed. This puts the infant at greater risk for atelectasis because airway closure can occur even during tidal breathing.24The closing volume plus the residual volume constitutes the closing capacity. If FRC is decreased relative to closing capacity, this converts normal areas of lung to low VA/Q areas and compounds the propensity for development of atelectasis.90 

Body Habitus.

Obesity worsens arterial oxygenation through multiple mechanisms,91of which development of atelectasis is an important contributor. This is because of a markedly reduced FRC promoting airway closure to a greater extent than in healthy-weight subjects.92As the weight of the torso and abdomen make diaphragmatic excursions more difficult—especially when recumbent or supine—the FRC decreases, and this is intensified in the setting of diaphragmatic paralysis associated with neuromuscular blockade. Don et al.  55further clarified the effect of body size on gas exchange and showed that an individual with an increased weight/height ratio (i.e. , obese) would be at a particular disadvantage in the supine position because closing volume is increased in relation to FRC. Pelosi et al.  93also investigated the effects of body mass index on FRC, respiratory mechanics, and gas exchange during general anesthesia. They found that with increasing body mass index (i.e. , ratio of body weight/surface area), FRC and lung compliance decreased, and the oxygenation index (Pao2/Pao2) decreased exponentially.93Prone positioning, although difficult in obese patients, may improve oxygenation.63Consistent with the effects of obesity, the reduced FRC that occurs during pregnancy also potentiates atelectasis.94 

Tidal Volume.

The ARDSnet study recommends the use of low tidal volume in patients with ARDS.95Lower tidal volume reduces stretch-induced lung injury in patients with ARDS,96and this approach is translated into improved patient survival.95,97However, extrapolation of the low-tidal-volume approach to patients without lung injury (or ARDS) requires caution for two principal reasons. First, it has been long recognized that low tidal volume increases the development of atelectasis in the absence of lung injury.2,98–100Therefore, generalized adoption of low tidal volume in patients without preexisting lung injury (e.g. , during general anesthesia) could promote development of atelectasis. Second, in the presence of ARDS, the ARDSnet protocol is specific: The data stipulate 6 ml/kg (vs.  12 ml/kg) in the context of a precise ventilatory management protocol that stipulates many ventilatory parameters, in addition to tidal volume.95A recent study has suggested that the specific “low-tidal-volume” approach used in the ARDSnet study95was actually associated with the development of intrinsic PEEP,97raising the possibility that recruitment—not simply low tidal stretch—played a protective role in these patients. Therefore, if a low tidal volume strategy is used that does not result in the development of intrinsic PEEP, the propensity for development of atelectasis might be significant. The use of low tidal volume in the absence of recruitment or PEEP in anesthetized patients without lung injury may lead to atelectasis and is not recommended.

Two practical points are important regarding mode of ventilation during general anesthesia. In contrast to volume-controlled ventilation, pressure-controlled ventilation results in smaller delivered tidal volumes when respiratory system compliance is decreased (e.g. , during surgical retraction or in the presence of abdominal packs). Smaller tidal volumes may lead to atelectasis and may go undiagnosed because there is no change in the peak airway pressure as pressure-controlled ventilation is being used. In addition, fresh gas flow may have an impact because with older volume-controlled ventilators, increased fresh gas flow results in increased delivered tidal volume.101 

Preexisting Lung Disease.

Smokers and patients with lung disease show more pronounced gas exchange impairment in the awake state than healthy subjects do, and this difference also persists during anesthesia.102However, only a small shunt and almost no atelectasis develops in these patients, but they may have severe VA/Q mismatch. Hyperinflation of the lungs may make them resist collapse.103The chronic hyperinflated state of the lungs in chronic bronchitis changes the mechanical behavior of the lungs and the interaction with the chest wall so that the tendency to collapse is reduced. However, patients with chronic obstructive lung disease may have large regions with low VA/Q ratios that can result, over time, in resorption atelectasis.4 

Effects of Atelectasis

Development of atelectasis is associated with the development of several pathophysiologic effects, including decreased compliance, impairment of oxygenation, increased pulmonary vascular resistance, and development of lung injury.

Decreased Compliance.

One of the first articles examining the effects of atelectasis was by Mead and Collier99in 1959. They noted that when anesthetized dogs were allowed to breathe spontaneously or were paralyzed and ventilated at tidal volumes of approximately 12.5 ml/kg, pulmonary compliance decreased progressively. They found that these changes were immediately reversed after forced inflations of the lungs, whereas forced deflations caused further compliance reductions. The appearance of the lungs as well as measurement of total and ventilatory lung volumes indicated that the lungs were atelectatic.99 

These laboratory findings were translated into the perioperative context with the article by Bendixen et al. ,2which reported that atelectasis caused a decrease in pulmonary compliance in surgical patients and was associated with a worsening in systemic oxygenation. The decreased compliance is conventionally considered to be due to a reduction in lung volume, such that inspiration–expiration cycles commencing from a lower FRC are completed on a less efficient section of the notional pressure–volume curve.104Therefore, greater energy is consumed because a given change in transpulmonary pressure results in a lesser tidal volume because of the sigmoid shape of the pressure–volume curve. An anatomical basis has been suggested for such atelectasis-associated decreased FRC in the context of general anesthesia (see Compression Atelectasis).6 

The pressure–volume characteristics of the lung determine the work of breathing, and ventilatory work may be analyzed by plotting pressure against volume.105In the presence of increased airway resistance or decreased lung compliance, increased transpulmonary pressure is required to achieve a given tidal volume with consequent increase in the work of breathing.

Although the concept of altered compliance has been well established in the setting of “macroatelectasis” (e.g. , lobar or dependent atelectasis sufficiently large to be radiologically apparent), there are no data regarding whether microatelectasis (e.g. , after brief exposure to increased Fio2during preoxygenation75) has comparable effects on lung mechanics.

Impaired Oxygenation.

In many situations, the most striking effect of atelectasis is impairment of systemic oxygenation. This was first identified in the context of general anesthesia2where the use of passive hyperinflations reversed the hypoxemia.2Others reported impairment of oxygenation during prolonged constant-volume ventilation using small tidal volumes in the absence of intermittent hyperinflations.106–108 

Atelectasis can occur as a result of hyperoxia.75,109If high Fio2is continued, the effects may not be noted by observing pulse oximetry, but only if Pao2is measured. In this situation, the impaired oxygenation can be expressed in terms of Pao2. The cause of the impaired oxygenation has been shown, using the multiple inert gas technique, to result from increased mismatch of ventilation with perfusion.75 

Two approaches have been shown to mitigate against the development of hypoxia. First, as demonstrated originally, intermittent hyperinflation maneuvers reverse the effect on gas exchange.2Maintenance of lung volume from the outset can prevent, as opposed to reverse, development of intraoperative atelectasis.28Second, although recognized as an issue for decades, the composition of the inspired gases used during induction of general anesthesia has been shown to directly impact the development of microatelectasis in healthy patients undergoing general anesthesia,75as well as in patients with lung injury.110Rothen et al.  75found that very little atelectasis occurred after the induction of general anesthesia in subjects whose lungs were ventilated with 30% oxygen in nitrogen. Furthermore, the increase in the amount of atelectasis was less rapid in the setting of 30% oxygen (in nitrogen) compared with 100% oxygen. This is consistent with the notion that a poorly absorbed gas such as nitrogen might prevent the early formation of atelectasis and, conversely, that use of a highly absorbed gas (e.g. , oxygen) would enhance the development of atelectasis.

Pulmonary Vascular Resistance.

Early studies suggested that the pulmonary vascular resistance was minimal at FRC. Lung volume much above this notional value resulted in alveolar compression due to lung stretch, whereas lung volume falling below the FRC was thought to result in compression of extraalveolar vessels. Therefore, this notion explained the changes in pulmonary vascular resistance on the basis of physical alteration of the pulmonary blood vessels, either stretching or narrowing caused by increased lung volume or compression caused by decreased lung volume.111–113However, regional hypoxia develops in atelectatic lungs, and it has been shown that the mechanism of increased large vessel pulmonary vascular resistance in the lungs is due to hypoxic pulmonary vasoconstriction, due in turn to decreased alveolar and mixed venous oxygen tension.114–116Recent work by our group has demonstrated that this significant increase in vascular resistance can occur in previously normal lungs in an experimental setting, resulting in right ventricular dysfunction and increased microvascular leakage.117 

Lung Injury.

Extensive evidence has established the importance of maintenance of lung volume in the prevention of lung injury. The pivotal publication by Webb and Tierney118demonstrated that application of PEEP prevented the development of lung injury induced by extremely high tidal volume. The specific degree of atelectasis responsible for attenuation or prevention of high tidal volume–induced lung injury was explored by Sandhar et al.  119and Muscedere et al.  120using different experimental models over 5- and 2-h time periods, respectively. In isolated, nonperfused lungs that are ventilated with no or low PEEP, reductions in compliance and evidence of morphologically apparent lung injury occur. Permitting such atelectasis in the presence of high tidal volumes is associated with hyaline membrane formation, along with regional inhomogeneity of atelectasis and overdistension. Other articles have also demonstrated that repetitive lung collapse or atelectasis leads to increased neutrophil activation in previously injured lungs.121,122In addition to lung injury induced by extremely high tidal volumes, ventilation at low lung volumes worsens lung injury by repeated small airway closure.123,124The concept of permissive hypercapnia developed to avoid lung injury caused by high tidal volumes or high inflation pressures. Higher end-tidal carbon dioxide levels may be accepted to reduce volutrauma or barotrauma, particularly in pediatric patients.

Potentiation of lung injury by atelectasis has additional implications for inflammatory effects in the lung. Tremblay et al.  125examined the effect of ventilation strategy on lung inflammatory mediators in the presence and absence of lung injury and demonstrated that in the absence of PEEP, an impairment in lung compliance was accompanied by increased cytokine concentrations (e.g. , tumor necrosis factor α, interleukin 1β) that were greatest in the groups pretreated with lipopolysaccharide.125These concepts were extended to the in vivo  setting, where it was reported that maximal serum cytokine concentrations induced by high tidal volume occurred in the context of zero PEEP. In addition, atelectasis worsened the impairment of compliance induced by high tidal volume.126Perhaps of greatest concern in that publication was the high mortality (in the absence of cytokine alterations) observed in the in vivo  combination of low-tidal-volume ventilation in the presence of atelectasis. These data suggest that in terms of the most meaningful outcome (i.e. , survival), the combination of low tidal volume and atelectasis may be the most adverse ventilation strategy and that the increased cytokines observed in the high-tidal volume groups may be of less importance.126 

Recent work by our group, wherein rats without lung injury received ventilatory strategies with and without PEEP and recruitment maneuvers, may place these findings into perspective.117We found decreased survival in the zero-PEEP group and also demonstrated ultrastructural evidence of microvascular epithelial disruption in those animals. In addition, we demonstrated that right ventricular dysfunction, possibly secondary to increased pulmonary vascular resistance, occurred in the presence of reduced FRC.117 

Clinical Impact of Atelectasis beyond the Operating Room.

Development of atelectasis intraoperatively is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance, and development of lung injury. The adverse effects of atelectasis persist in the postoperative period and can impact patient recovery. Atelectasis can persist for 2 days after major surgery.127Often, the lung dysfunction is transient, and normal lung function resumes soon after anesthesia and surgery. For example, atelectasis resolves within 24 h after laparoscopy in nonobese subjects.128Nevertheless, patients experience perioperative respiratory complications that may be related to reduction in FRC.129,130 

Some pulmonary complications occur during or immediately after anesthesia—mainly hypoxemia. In a large study with more than 24,000 patients, 0.9% had a hypoxemic event in the postanesthesia care unit that necessitated a specific intervention other than only supplemental oxygen.131There is no clear evidence that atelectasis is the cause of all of these postoperative hypoxemic events; respiratory depression from residual anesthetic may be more likely.24However, it seems likely that preventing atelectasis formation during the whole perioperative period would increase the pulmonary oxygen reserve, potentially reducing the likelihood of late postoperative complications.

The characteristic postoperative mechanical respiratory abnormality after abdominal or thoracic surgery is a restrictive pattern with severely reduced inspiratory capacity, vital capacity, and FRC.132–134Patients breathe rapidly with small tidal volumes and are unwilling—or unable—to inspire deeply. Patients in whom postoperative pulmonary complications develop have a relatively greater reduction of FRC, vital capacity, and Pao2than those who do not.132,134The impact of postoperative pain control in preventing postoperative atelectasis has been the focus of much research effort. Although pain and muscle splinting in response to pain are traditionally assumed to be the principal causative factors, total relief of pain after upper abdominal surgery—using epidural analgesia—results in only partial restoration of vital capacity and has minimal effect on FRC.135However, a recent meta-analysis suggested that postoperative epidural opioids significantly decrease the frequency of atelectasis but not other pulmonary complications when compared with systemic opioids.136Other studies have found no difference in the incidence of pulmonary complications. Manikian et al.  137demonstrated that thoracic epidural analgesia in 13 patients undergoing upper abdominal surgery caused a significant increase in forced vital capacity, but the FRC remained unchanged. Spence and Logan138reported no significant impact of postoperative epidural analgesia on oxygenation when compared with patients receiving systemic morphine, and Jayr et al.  139reported that although the epidural provided superior postoperative analgesia, it did not affect the frequency of postoperative pulmonary complications, regardless of preoperative pulmonary status. Finally, a recent multicenter randomized trial of 915 high-risk surgical patients reported a slight reduction in postoperative pulmonary complications—but no impact on mortality or major morbidity—attributable to epidural versus  systemic analgesia, although this study may have been underpowered to examine mortality.140 

Two particular aspects of pulmonary defense mechanisms, coughing and removal of particulate matter, are adversely affected by the changes in lung mechanics and breathing pattern135; this may predispose to pulmonary infection. A number of studies examined the effects of halothane and thiopentone on mucociliary clearance and found that these agents may be responsible for reduced mucous clearance in the postoperative period.141–143A more recent study demonstrated that total intravenous anesthesia with propofol, alfentanil, and vecuronium depressed mucociliary flow in patients with healthy lungs.144Cervin and Lindberg145examined the effects of desflurane on mucociliary activity in the rabbit maxillary sinus in vivo . Desflurane increased mucociliary activity, and the authors concluded that desflurane is an airway irritating compound.145Atelectasis and pneumonia are often considered together because the changes associated with atelectasis may predispose to pneumonia.146Despite a direct lack of evidence of a correlation between atelectasis and pneumonia, reducing or avoiding atelectasis may diminish postoperative pulmonary complications147and thus improve outcome; however, this remains to be proven.

In a series of adults undergoing elective abdominal surgery, postoperative pulmonary complications occurred in 9.6% of cases.148Atelectasis and infectious complications account for the majority of reported pulmonary complications,149and the consequences include a significant burden in terms of morbidity149and additional healthcare costs.150In some series, pulmonary complications account for 24% of deaths within 6 days of surgery,130,149although the precise relation to atelectasis is unclear.

Experimental Evidence that Atelectasis Causes Lung Injury.

The majority of studies examining the interactions of mechanical ventilation and nonventilatory lung injury have observed the effects of injurious mechanical ventilation strategy on preinjured lungs. However, several experimental studies have examined the effect of preemptive recruitment on the effects of subsequent lung injury.

Atelectasis Worsens Lung Injury Caused by Mechanical Stretch.

Multiple studies have convincingly demonstrated that recruitment provides effective protection against lung injury that is either induced118,151,152or aggravated120,125,153,154by mechanical stretch. This may assume increasing importance as the role of tidal volume and plateau pressures in ARDS is debated.95,155,156 

Atelectasis Worsens Lung Injury Not Caused by Mechanical Stretch.

Most patients with severe lung injury require supportive mechanical ventilation. It is clear from multiple laboratory157,158and clinical95,159studies that stretch can cause or worsen lung injury. However, there is a vast spectrum of causes of ALI, and there are striking similarities—and few differences—in the pathogenesis, pathophysiologic dysfunction, and histologic appearance of ALI or ARDS, whether caused by stretch158or other etiologies.160Therefore, because recruitment is effective in reducing stretch-induced injury and because so many pathogenic and morphologic features are shared between stretch-induced versus  other forms of injury, it may be that the protective effects of recruitment could be applicable to lung injury that is not caused by increased tidal stretch.

Additional specific lines of evidence exist. Inflation of a lung graft before reimplantation, as opposed to maintenance of the lung in a deflated state, confers increased viability.161–163The importance of inflation in lung protection has been confirmed in in vivo  162,163and ex vivo  161models and may be mediated either via  reduction in pulmonary vascular resistance161(potentially decreasing endovascular shear injury) or through prevention of surfactant inactivation.163Finally, early application of mechanical ventilation may, through maintenance of lung volume (FRC), reduce mortality in experimental porcine sepsis164and in experimental hemorrhagic shock.165 

Detection of Atelectasis

Atelectasis is usually suspected when alterations in lung physiology consistent with the development of atelectasis (e.g. , decreased compliance, impaired oxygenation) occur in a setting where atelectasis is likely. However, confirmation of atelectasis is possible through a variety of means.

Conventional Chest Radiography.

Lobar or segmental atelectasis is classically represented as opacification of the lobe or lobar segment in question. General signs of atelectasis relate to volume loss. The most direct and reliable sign is the displacement of the interlobar fissure. Other signs of volume loss, such as increase of the hemidiaphragm and mediastinal shift, are maximal nearest the point of volume loss. Compensatory overinflation of the remaining aerated segments in the affected lobe is present, and the collapsed portion of the lung is of increased opacity and often triangular in at least one projection.166For example, when atelectasis results from proximal bronchial occlusion, an obstruction may be identifiable in the proximal bronchial tree, beyond which the tree is not aerated. If atelectasis results from absorption, the features are similar to consolidation, where the atelectatic lung parenchyma is opacified, and contrasts with the patent bronchial airway.

In addition to airway characteristics, other features of atelectasis are important. The “silhouette” sign allows identification of the lobe or segment of the lung that is affected. It is based on the principle that apposition of densely atelectatic lung with an additional contiguous structure, such as the diaphragm or the heart, results in obliteration of the boundary between the lung and the adjacent structure. For example, opacification of part of an atelectatic lung in conjunction with obliteration of the ipsilateral hemidiaphragm suggests lower lobar atelectasis; in contrast, preservation of the hemidiaphragm indicates that the ipsilateral lower lobe is not atelectatic.

A cardinal characteristic of atelectasis is volume loss of the affected lobe. This is associated with secondary changes in adjacent structures, in an attempt to “fill the gap” created by the loss of lung volume, and results in alterations including shift of the mediastinum or the hilum towards the affected area, elevation of the ipsilateral hemidiaphragm, and secondary (or “compensatory”) emphysema in the adjacent nonatelectatic lung.

There is no doubt that conventional chest radiographs can reveal collapse in a segmental or lobar distribution. However, the ability of chest radiographs to detect atelectasis that occurs during general anesthesia or during mechanical ventilation of recumbent critically ill patients is less certain.167 

Computed Tomography.

Computed tomography is emerging as the preferred method for imaging the lung because of the widespread availability, resolution, high signal/noise ratio for lung tissue, and speed. From conventional CT images, it is possible to measure whole and regional lung volumes, distribution of lung aeration, and recruitment behavior under various clinical conditions and interventions.168In the 1980s, atelectasis was shown by CT in anesthetized patients.5,169 

Since then, atelectasis has been studied extensively. Atelectasis on a CT scan has been defined as pixels with attenuation values of −100 to +100 Hounsfield units.3Hounsfield units quantify attenuation or density seen on CT. In this study, Lundquist et al.  3studied patients undergoing elective abdominal surgery with CT of the thorax during anesthesia. Attenuation values in histograms of the lung and atelectasis were studied using two methods of calculating the atelectatic area. On the basis of the CT findings, atelectasis occurs in the most dependent parts of the lungs and occurs in almost 90% of patients who are anesthetized. The extent of the atelectasis in the dependent regions can be reduced by PEEP.5 

The lung in ARDS is characterized by a marked increase in lung tissue and a massive loss of aeration.170Gattinoni et al.  40,41,171,172have extensively investigated the distribution of tidal volume and recruitment in patients with ARDS using CT scans. They concluded that PEEP makes the gas distribution more homogenous in patients with ARDS, stretching the upper levels and recruiting the lower ones, and thereby reduces the atelectatic tissue in dependent regions. Rouby173has assessed PEEP-induced lung overdistension using CT. Rouby determined the threshold to differentiate PEEP-induced alveolar recruitment from PEEP-induced lung overdistension. The threshold of 900 Hounsfield units allows a reliable determination of PEEP-induced alveolar overdistension. A number of human studies have clearly reported the simultaneous onset of alveolar recruitment and lung overinflation in patients receiving PEEP levels of 10 and 20 cm H2O.174–177These recent approaches have important implications in the diagnosis as well as the management of atelectasis because they point clearly to the propensity for injurious regional overinflation occurring as a result of efforts to reverse atelectasis (e.g. , increased PEEP, recruitment maneuvers) in the setting of ARDS.

Magnetic Resonance Imaging.

Magnetic resonance imaging allows three-dimensional imaging without the use of ionizing radiation. Unfortunately, the lung is not well suited to magnetic resonance imaging. On spin-echo images in healthy subjects, little signal is obtained from lung parenchyma. Areas of consolidation and masses can be identified, but the degree to which they can be differentiated has yet to be fully established. This technique has been used in preterm neonates to study pulmonary dysfunction.178The authors compared lung water content and distribution between preterm and term infants and concluded that lung water content is higher in preterm infants, consistent with dependent atelectasis.178Xenon-enhanced CT is a method for noninvasive measurement of regional pulmonary ventilation, determined from the wash-in and wash-out rates of the radiodense, nonradioactive xenon gas, measured by serial CT scans.179This may provide a valuable tool for noninvasive measurement of regional lung function and atelectasis in the future. Although magnetic resonance has several advantages over CT (e.g. , contrast material is not necessary, possibility for multiple planar imaging), it is not apparent that magnetic resonance offers any distinct advantages over CT in the evaluation of atelectasis at the current time.180 


Although more commonly used in assessment of pleural collections or in the context of echocardiography, thoracic ultrasonography has been used in assessment of lung parenchyma.181It has been suggested as a useful aid to the rapid diagnosis of atelectasis182and, in the context of ARDS, seems to be useful for the assessment of regional consolidation.183Recently, use of a specific ultrasonographic detection of the cardiac impulse, termed the lung pulse , has been reported to be a highly sensitive early indicator of the presence of atelectasis.184The use of ultrasonography may offer significant advantages for patients in the operating room or in the intensive care unit in terms of rapidity and ease of examination, without the disadvantages of patient transport and radiation exposure. However, its role in clinical practice remains to be determined.185 

Intravital Microscopy.

Intravital microscopy applied to the pleural surface enables experimental visualization of atelectasis and examination of its role in the pathogenesis of lung injury (see Direct Visualization of Atelectasis).31In addition to access issues, there are limitations to interpretation,32including the fact that visualization is restricted to lung tissue that is immediately below the pleural surface, with deeper parenchyma beyond the range of the instrument.

Cytokine Profile.

There are other methods of detecting atelectasis in the preclinical setting, including lung lavage levels of cytokines.125Tremblay et al.  125examined the effect of ventilation strategy on lung inflammatory mediators in the presence and absence of lung injury using an isolated rat model. Lung lavage cytokine concentrations were greatest in the groups ventilated without PEEP in both the control intravenous lipopolysaccharide–treated groups. Zero PEEP in combination with high volume ventilation had a synergistic effect on cytokine concentrations. This finding that atelectasis worsens stretch-induced lung injury resulting in increased lung and systemic cytokine concentrations was confirmed by Chiumello et al.  126However, it is important to note that experimental atelectasis—even when lethal—is not associated with increased cytokines in the absence of high tidal volumes.126The measurement of lung lavage levels of cytokines in the clinical situation is impractical.

Prevention or Reversal of Atelectasis

The factors important in the prevention or reversal of atelectasis differ considerably, depending on whether the lungs are injured or uninjured. Because of the adverse pathophysiology associated with the development of atelectasis and the preclinical findings that recruitment of atelectatic lung may reduce the propensity toward subsequent injury,161–163it is important to examine how recruitment may be achieved.

Prevention or Reversal of Atelectasis in Healthy Lungs.

Progressive pulmonary atelectasis (and the associated impairment of oxygenation) may occur during constant ventilation whenever periodic hyperinflation is lacking; it is reversible by passive hyperinflation (i.e. , three successive inflations: first, with a pressure of 20 cm H2O for 10 s; second, with a pressure of 30 cm H2O for 15 s; and third, with a pressure of 40 cm H2O sustained for 15 s).2This was taken as evidence that atelectatic alveoli are reopened by the deep breaths, and that conclusion was supported by the reduction in pulmonary compliance occurring during ventilation and the return of compliance to control values after hyperinflation.

Nunn et al.  107examined arterial oxygenation in patients during routine anesthesia. They found that arterial oxygenation increased when a pressure of 40 cm H2O was maintained for 40 s; lower pressures, even with modest levels of PEEP, were not effective.107A more recent study by Tusman et al.  28examined an “alveolar recruitment” strategy in healthy lungs during general anesthesia. The authors hypothesized that because atelectasis occurs during general anesthesia, an initial increase in pressure would be required to open collapsed alveoli, and if this inspiratory recruitment was combined with sufficient end-expiratory pressure, alveoli would remain open. They allocated patients to one of three groups: no PEEP; an initial control period without PEEP followed by PEEP of 5 cm H2O; and PEEP of 15 cm H2O with high tidal volume (18 ml/kg, or peak inspiratory pressure 40 cm H2O) maintained for 10 breaths, followed by stepwise reduction of PEEP and tidal volume. The third group, receiving the alveolar recruitment strategy, had a significant increase in arterial oxygenation during general anesthesia. Treatment with PEEP of 5 cm H2O alone did not have the same effect on oxygenation. The authors concluded that high initial pressures are needed to overcome the anesthesia-induced collapse and that PEEP of 5 cm or more is required to prevent the newly recruited alveoli from collapsing. In addition, there was no evidence of barotrauma or pulmonary complications as a result of the high initial airway pressures.28 

Prevention or Reversal of Atelectasis in Injured Lungs.

It has become evident that a number of ventilatory strategies can produce or worsen lung injury.157The use of large tidal volumes,153high peak airway pressures,186and end-expiratory alveolar collapse with cyclic reopening120have all been proposed as deleterious when ventilating injured lungs. Several studies have shown that lung injury secondary to ventilation with large tidal volume is attenuated if end-expiratory volume is maintained by the use of PEEP.118,126,152In addition, ventilation at low FRC worsens lung injury, possibly by repeated small airway closure, and PEEP markedly attenuates this injury.120,126Therefore, recruitment of atelectatic lung reduces the injurious effects of mechanical ventilation with both low and high tidal volumes and protects against development of ventilator-induced lung injury.

The “open-lung” approach to ventilating patients with ARDS consists of a recruitment maneuver with high sustained airway pressures to open atelectatic alveoli followed by application of PEEP to maintain alveolar patency. This approach was among the interventions performed in a study that showed an improvement in oxygenation and reduced mortality in patients with ARDS.159The researchers calculated the inflection point from a pressure–volume curve (corresponding to an upward shift in the slope of the curve), and PEEP was preset at 2 cm H2O above the inflection point in the protective ventilation group. If the inflection point could not be determined on the pressure–volume curve, PEEP of 16 cm H2O was used. Recruiting maneuvers were frequently used and consisted of continuous positive airway pressures of 35–40 cm H2O for 40 s followed by a return to previous PEEP levels.159 

Gattinoni et al.  40also showed that with increasing PEEP from 0 to 20 cm H2O, gas distribution became more homogenous in sedated and paralyzed patients with ARDS and reduced the reopening–collapsing tissue. Suter et al.  187suggested that the optimum end-expiratory pressure in patients with acute respiratory failure was the PEEP level that resulted in the greatest total static compliance. This maximum compliance produced by PEEP resulted in optimum overall cardiopulmonary interaction to ensure maximal global oxygen delivery. In patients with low FRC values at zero end-expiratory pressure, maximum oxygen transport was achieved at higher levels of PEEP than in patients with normal or high FRC values.

The timing of recruitment maneuvers was examined by Grasso et al.  188in patients with ARDS who were ventilated with a lung-protective ventilatory strategy (low tidal volumes of 6 ml/kg). They defined a recruiting maneuver as continuous positive airway pressure of 40 cm H2O for 40 s. Measurements of Pao2/Fio2ratio, volume–pressure curve, and respiratory mechanics were obtained 2 and 20 min after application of a recruiting maneuver. The authors classified the patients as responders and nonresponders. Recruitment maneuvers increased the Pao2/Fio2ratio significantly more in responders—who had been ventilated for a longer period of time—than in nonresponders. The authors concluded that application of recruiting maneuvers improves oxygenation only in patients with early ARDS who do not have impairment of chest wall mechanics and with a large potential for recruitment.188 

Treating Atelectasis in the Postoperative Period.

Postoperative pulmonary complications are increasingly recognized as an important perianesthetic issue.146Determination of the frequency and clinical impact of postoperative pulmonary complications is hampered by the lack of a uniform definition of a postoperative pulmonary complication among studies. Included in the definition are pneumonia, severe respiratory failure (usually defined as the need for mechanical ventilation), bronchospasm, and atelectasis (often not defined). Most studies referring to postoperative atelectasis do not directly measure FRC.

Reversing or preventing atelectasis is possible in many patients in the perioperative period146,189and is of proven benefit in preventing pulmonary complications.146Techniques or devices that either encourage or force patients to inspire deeply are of most clinical importance.190–192The aim is to produce a large and sustained increase in transpulmonary pressure distending the lung and reexpanding collapsed lung units. Several methods have been studied, including intermittent positive-pressure breathing, deep-breathing exercises, incentive spirometry, and chest physiotherapy. A meta-analysis suggests that all regimens studied are equally efficacious in reducing the frequency of postoperative pulmonary complications after upper abdominal surgery.193 

The beneficial effect on gas exchange of a simple posture change from supine to seated has been demonstrated, both in healthy subjects90and after upper abdominal surgery.91Identification of FRC as the single most important lung volume in postoperative patients provides a specific goal of therapy.189FRC can be measured by a number of techniques. Gas dilution techniques (e.g. , helium equilibration, nitrogen washout) have been used.93,194One disadvantage of these methods is that the tracer gas may not mix with all gas in the lungs because of occluded airways; this source of error can be overcome by using body plethysmography.

Finally, early work reported the use of thoracic or sternal traction195,196as well as the use of intravenous aminophylline197as successful treatments of atelectasis in a number of case reports, but given the impracticalities and adverse effects of these therapies, they have no clinical application today.

Recruitment of Atelectatic Lung Is Easier to Achieve in the Absence of Injury.

Although the pressure–volume relation in ARDS—and the ability to recruit lung—may depend on the etiology,171it is always easier to recruit lung when injury is absent or mild, compared with when significant injury is established.42,188,198This is because the uninjured lung is highly compliant, and its inflection point (opening pressure) on the inflation pressure–volume curve is either low or not detectable. In contrast, the inflection point is significantly greater when injury has been established; in fact, elevation of the inflection point increases in proportion to the extent of injury.194Such impaired compliance (and difficulty with recruitment) has a pathophysiologic basis in established injury. The causes include surfactant dysfunction due to impairment of large aggregate formation,199direct inhibition by plasma proteins that have exudated into the air space,200–202and the progression of cellular infiltration and edema in the pulmonary interstitium and alveoli.203,204Increases in pulmonary vascular resistance, which characteristically parallel the progression of the lung injury,205may decrease lung compliance further.206Finally, when recruitment has been achieved, less airway pressure is required to prevent derecruitment than is required to achieve recruitment.207 

In the future, clinicians may be able to predict the subsequent development of ALI. In an optimal setting, this would be after recognition of the identifiable etiology and before its initiation (e.g. , before major surgery or before reperfusion during transplantation surgery). Alternatively, early institution of prophylactic recruitment after identification of an etiologic event, particularly when associated with a worrisome predictive stratification (e.g. , pancreatitis with elevated cytokine profile), would be ideal. The eventual prospect of predicting (or early detection of) ALI and ARDS makes “prophylactic lung recruitment” (to maintain or recover normal resting lung volume) increasingly tenable, and if validated by clinical studies, this could become integrated into the perioperative care of patients who are at risk of developing critical illness.

Atelectasis occurs in almost all patients undergoing general anesthesia. We have reviewed the causes, effects, nature, identification, and prevention of atelectasis in the perioperative period. Unless restoration of FRC takes place, atelectasis can have detrimental consequences. Current literature indicates that intraoperative and postoperative lung recruitment improves intermediate physiologic outcomes (e.g. , oxygenation, work of breathing); however, the benefits might have more significant implications for lung injury and ARDS. Low stretch ventilation can achieve, at best, attenuation of stretch-induced injury; at worst, it can cause loss of lung volume, potentially contributing to or worsening injury. Prophylactic recruitment however, could reduce or prevent lung injury that results from a variety of primary etiologies, as well as reducing injury resulting from mechanical stretch. If proven in the clinical setting, this approach could reduce the development of critical illness in many general medical and surgical patient populations.

Since acceptance of this manuscript, Squadrone et al . have demonstrated that reversing atelectasis with noninvasive continuous positive airway pressure in high-risk postoperative patients who are hypoxic results in reduced need for reintubation and a lower incidence of pneumonia and sepsis (Squadrone V, Coha M, Cerutti E, Schellino MM, Biolino P, Occella P, Belloni G, Vilianis G, Fiore G, Cavallo F, Ranieri VM; Piedmont Intensive Care Units Network [PICUN]: Continuous positive airway pressure for treatment of postoperative hypoxemia: A randomized controlled trial. JAMA 2005; 293:589–95).

The authors thank Steven Deem, M.D. (Associate Professor, Departments of Anesthesiology and Medicine, University of Washington, Seattle, Washington), Rolf Hubmayr, M.D. (Professor, Department of Medicine, Mayo Clinic, Rochester, Minnesota), and John Laffey, M.D. (Consultant Anesthetist, University Hospital and National University of Ireland, Galway, Ireland), for their expert comments on the manuscript; and Theresa Sakno (Sakno Media, Toronto, Ontario, Canada) for the artwork.

Nunn JF, Payne JP: Hypoxaemia after general anaesthesia. Lancet 1962; 2:631–2
Bendixen HH, Hedley-Whyte J, Chir B, Laver MB: Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. N Engl J Med 1963; 269:991–6
Lundquist H, Hedenstierna G, Strandberg A, Tokics L, Brismar B: CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995; 36:626–32
Hedenstierna G, Rothen HU: Ventilation and perfusion matching, Anesthesia Biologic Foundations. Edited by Yaksh TL, Lynch CL, Zapol WM, Maze M, Biebuyck JF, Saidman LJ. Philadelphia, Lippincott–Raven, 1998, pp 1349–66Yaksh TL, Lynch CL, Zapol WM, Maze M, Biebuyck JF, Saidman LJ
Brismar B, Hedenstierna G, Lundquist H, Strandberg A, Svensson L, Tokics L: Pulmonary densities during anesthesia with muscular relaxation: A proposal of atelectasis. Anesthesiology 1985; 62:422–8
Froese AB, Bryan AC: Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 1974; 41:242–55
Nunn JF: Nunn’s Applied Respiratory Physiology, 3rd edition. London, Butterworth Heinemann, 1987, pp 350–70
Butterworth Heinemann
Hedenstierna G, Strandberg A, Brismar B, Lundquist H, Svensson L, Tokics L: Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology 1985; 62:247–54
Krayer S, Rehder K, Beck KC, Cameron PD, Didier EP, Hoffman EA: Quantification of thoracic volumes by three-dimensional imaging. J Appl Physiol 1987; 62:591–8
Hubmayr RD, Rodarte JR, Walters BJ, Tonelli FM: Regional ventilation during spontaneous breathing and mechanical ventilation in dogs. J Appl Physiol 1987; 63:2467–75
Benameur M, Goldman MD, Ecoffey C, Gaultier C: Ventilation and thoracoabdominal asynchrony during halothane anesthesia in infants. J Appl Physiol 1993; 74:1591–6
Hedenstierna G, Tokics L, Lundquist H, Andersson T, Strandberg A, Brismar B: Phrenic nerve stimulation during halothane anesthesia: Effects of atelectasis. Anesthesiology 1994; 80:751–60
Loring SH, Butler JP: Gas exchange in body cavities, Handbook of Physiology. Section 3, The Respiratory System. Vol 4, Gas Exchange. Edited by Farhi LE, Tenney SM. Bethesda, American Physiological Society, 1987, pp 283–95Farhi LE, Tenney SM
American Physiological Society
Joyce CJ, Baker AB, Kennedy RR: Gas uptake from an unventilated area of lung: Computer model of absorption atelectasis. J Appl Physiol 1993; 74:1107–16
Rehder K, Knopp TJ, Sessler AD, Didier EP: Ventilation-perfusion relationship in young healthy awake and anesthetized-paralyzed man. J Appl Physiol 1979; 47:745–53
Wagner PD, Laravuso RB, Uhl RR, West JB: Continuous distributions of ventilation-perfusion ratios in normal subjects breathing air and 100 per cent O2. J Clin Invest 1974; 54:54–68
Woo SW, Berlin D, Hedley-Whyte J: Surfactant function and anesthetic agents. J Appl Physiol 1969; 26:571–7
Wollmer P, Schairer W, Bos JA, Bakker W, Krenning EP, Lachmann B: Pulmonary clearance of 99mTc-DTPA during halothane anaesthesia. Acta Anaesthesiol Scand 1990; 34:572–5
Nicholas TE, Barr HA: The release of surfactant in rat lung by brief periods of hyperventilation. Respir Physiol 1983; 52:69–83
Hildebran JN, Goerke J, Clements JA: Surfactant release in excised rat lung is stimulated by air inflation. J Appl Physiol 1981; 51:905–10
Oyarzun MJ, Clements JA: Ventilatory and cholinergic control of pulmonary surfactant in the rabbit. J Appl Physiol 1977; 43:39–45
Oyarzun MJ, Clements JA: Control of lung surfactant by ventilation, adrenergic mediators, and prostaglandins in the rabbit. Am Rev Respir Dis 1978; 117:879–91
Oyarzun MJ, Iturriaga R, Donoso P, Dussaubat N, Santos M, Schiappacasse ME, Lathrop ME, Larrain C, Zapata P: Factors affecting distribution of alveolar surfactant during resting ventilation. Am J Physiol 1991; 261:L210–7
Magnusson L, Spahn DR: New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003; 91:61–72
Strandberg A, Hedenstierna G, Tokics L, Lundquist H, Brismar B: Densities in dependent lung regions during anaesthesia: Atelectasis or fluid accumulation? Acta Anaesthesiol Scand 1986; 30:256–9
Hedenstierna G, Lundquist H, Lundh B, Tokics L, Strandberg A, Brismar B, Frostell C: Pulmonary densities during anaesthesia: An experimental study on lung morphology and gas exchange. Eur Respir J 1989; 2:528–35
Tusman G, Bohm SH, Vazquez de Anda GF, do Campo JL, Lachmann B: “Alveolar recruitment strategy” improves arterial oxygenation during general anaesthesia. Br J Anaesth 1999; 82:8–13
Tusman G, Bohm SH, Tempra A, Melkun F, Garcia E, Turchetto E, Mulder PG, Lachmann B: Effects of recruitment maneuver on atelectasis in anesthetized children. Anesthesiology 2003; 98:14–22
Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G: Re-expansion of atelectasis during general anaesthesia: A computed tomography study. Br J Anaesth 1993; 71:788–95
Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G: Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesthesiol Scand 1995; 39:118–25
Halter JM, Steinberg JM, Schiller HJ, DaSilva M, Gatto LA, Landas S, Nieman GF: Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar collapse and recruitment/derecruitment. Am J Respir Crit Care Med 2003; 167:1620–6
Kavanagh BP: Lung recruitment in real time: Learning was never so easy. Am J Respir Crit Care Med 2003; 167:1585–6
West JB: Respiratory Physiology, 5th edition. Baltimore, Williams & Williams, 1995, pp 51–69
Williams & Williams
Baumgardner JE, Markstaller K, Pfeiffer B, Doebrich M, Otto CM: Effects of respiratory rate, plateau pressure, and positive end-expiratory pressure on PaO2 oscillations after saline lavage. Am J Respir Crit Care Med 2002; 166:1556–62
Williams EM, Viale JP, Hamilton RM, McPeak H, Sutton L, Hahn CE: Within-breath arterial PO2oscillations in an experimental model of acute respiratory distress syndrome. Br J Anaesth 2000; 85:456–9
Ludwigs U, Klingstedt C, Baehrendtz S, Wegenius G, Hedenstierna G: Volume-controlled inverse ratio ventilation in oleic acid induced lung injury: Effects on gas exchange, hemodynamics, and computed tomographic lung density. Chest 1995; 108:804–9
Mang H, Kacmarek RM, Ritz R, Wilson RS, Kimball WP: Cardiorespiratory effects of volume- and pressure-controlled ventilation at various I/E ratios in an acute lung injury model. Am J Respir Crit Care Med 1995; 151:731–6
Neumann P, Berglund JE, Mondejar EF, Magnusson A, Hedenstierna G: Effect of different pressure levels on the dynamics of lung collapse and recruitment in oleic-acid-induced lung injury. Am J Respir Crit Care Med 1998; 158:1636–43
Hubmayr RD: Perspective on lung injury and recruitment: A skeptical look at the opening and collapse story. Am J Respir Crit Care Med 2002; 165:1647–53
Gattinoni L, Pelosi P, Crotti S, Valenza F: Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med 1995; 151:1807–14
Gattinoni L, D’Andrea L, Pelosi P, Vitale G, Pesenti A, Fumagalli R: Regional effects and mechanism of positive end-expiratory pressure in early adult respiratory distress syndrome. JAMA 1993; 269:2122–7
Gattinoni L, Pesenti A, Avalli L, Rossi F, Bombino M: Pressure-volume curve of total respiratory system in acute respiratory failure: Computed tomographic scan study. Am Rev Respir Dis 1987; 136:730–6
Hubmayr RD, Walters BJ, Chevalier PA, Rodarte JR, Olson LE: Topographical distribution of regional lung volume in anesthetized dogs. J Appl Physiol 1983; 54:1048–56
Agostoni E, D’Angelo E, Bonanni MV: The effect of the abdomen on the vertical gradient of pleural surface pressure. Respir Physiol 1970; 8:332–46
D’Angelo E, Bonanni MV, Michelini S, Agostoni E: Topography of the pleural pressure in rabbits and dogs. Respir Physiol 1970; 8:204–29
Martynowicz MA, Minor TA, Walters BJ, Hubmayr RD: Regional expansion of oleic acid-injured lungs. Am J Respir Crit Care Med 1999; 160:250–8
Hedenstierna G, Jarnberg PO, Gottlieb I: Thoracic gas volume measured by body plethysmography during anesthesia and muscle paralysis: Description and validation of a method. Anesthesiology 1981; 55:439–43
Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G: Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiol Scand 1986; 30:154–8
Westbrook PR, Stubbs SE, Sessler AD, Rehder K, Hyatt RE: Effects of anesthesia and muscle paralysis on respiratory mechanics in normal man. J Appl Physiol 1973; 34:81–6
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 1987; 66:157–67
Freund FG, Bonica JJ, Ward RJ, Akamatsu TJ, Kennedy WF Jr: Ventilatory reserve and level of motor block during high spinal and epidural anesthesia. Anesthesiology 1967; 28:834–7
Ward RJ, Bonica JJ, Freund FG, Akamatsu T, Danziger F, Englesson S: Epidural and subarachnoid anesthesia: Cardiovascular and respiratory effects. JAMA 1965; 191:275–8
Yamakage M, Namiki A, Tsuchida H, Iwasaki H: Changes in ventilatory pattern and arterial oxygen saturation during spinal anaesthesia in man. Acta Anaesthesiol Scand 1992; 36:569–71
McCarthy GS: The effect of thoracic extradural analgesia on pulmonary gas distribution, functional residual capacity and airway closure. Br J Anaesth 1976; 48:243–8
Don HF, Wahba M, Cuadrado L, Kelkar K: The effects of anesthesia and 100 per cent oxygen on the functional residual capacity of the lungs. Anesthesiology 1970; 32:521–9
Don HF, Wahba WM, Craig DB: Airway closure, gas trapping, and the functional residual capacity during anesthesia. Anesthesiology 1972; 36:533–9
Lundh R, Hedenstierna G: Ventilation-perfusion relationships during anaesthesia and abdominal surgery. Acta Anaesthesiol Scand 1983; 27:167–73
Jonmarker C, Nordstrom L, Werner O: Changes in functional residual capacity during cardiac surgery. Br J Anaesth 1986; 58:428–32
Slocum HC, Hoeflich EA, Allen CR: Circulatory and respiratory distress from extreme positions on the operating table. Surg Gynecol Obstet 1947; 84:1065–7
Rehder K, Hatch DJ, Sessler AD, Fowler WS: The function of each lung of anesthetized and paralyzed man during mechanical ventilation. Anesthesiology 1972; 37:16–26
Lumb AB, Nunn JF: Respiratory function and ribcage contribution to ventilation in body positions commonly used during anesthesia. Anesth Analg 1991; 73:422–6
Rehder K, Knopp TJ, Sessler AD: Regional intrapulmonary gas distribution in awake and anesthetized-paralyzed prone man. J Appl Physiol 1978; 45:528–35
Gattinoni L, Tognoni G, Pesenti A, Taccone P, Mascheroni D, Labarta V, Malacrida R, Di Giulio P, Fumagalli R, Pelosi P, Brazzi L, Latini R: Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 2001; 345:568–73
Broccard AF, Shapiro RS, Schmitz LL, Ravenscraft SA, Marini JJ: Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model of acute respiratory distress syndrome. Crit Care Med 1997; 25:16–27
Broccard A, Shapiro RS, Schmitz LL, Adams AB, Nahum A, Marini JJ: Prone positioning attenuates and redistributes ventilator-induced lung injury in dogs. Crit Care Med 2000; 28:295–303
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 1997; 87:1153–63
Tenling A, Hachenberg T, Tyden H, Wegenius G, Hedenstierna G: Atelectasis and gas exchange after cardiac surgery. Anesthesiology 1998; 89:371–8
Macnaughton PD, Braude S, Hunter DN, Denison DM, Evans TW: Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass. Crit Care Med 1992; 20:1289–94
Claxton BA, Morgan P, McKeague H, Mulpur A, Berridge J: Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia 2003; 58:111–6
Dyhr T, Laursen N, Larsson A: Effects of lung recruitment maneuver and positive end-expiratory pressure on lung volume, respiratory mechanics and alveolar gas mixing in patients ventilated after cardiac surgery. Acta Anaesthesiol Scand 2002; 46:717–25
Loeckinger A, Kleinsasser A, Lindner KH, Margreiter J, Keller C, Hoermann C: Continuous positive airway pressure at 10 cm H2O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg 2000; 91:522–7
Benumof JL: Preoxygenation: Best method for both efficacy and efficiency. Anesthesiology 1999; 91:603–5
Krayer S, Rehder K, Beck KC, Cameron PD, Didier EP, Hoffman EA: Quantification of thoracic volumes by three-dimensional imaging. J Appl Physiol 1987; 62:591–8
Reber A, Engberg G, Wegenius G, Hedenstierna G: Lung aeration: The effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia 1996; 51:733–7
Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstierna G: Prevention of atelectasis during general anaesthesia. Lancet 1995; 345:1387–91
Benoit Z, Wicky S, Fischer JF, Frascarolo P, Chapuis C, Spahn DR, Magnusson L: The effect of increased FIO2before tracheal extubation on postoperative atelectasis. Anesth Analg 2002; 95:1777–81
Preoxygenation: Physiology and practice. Lancet 1992; 339:31–2
Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G: Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003; 98:28–33
Greif R, Akca O, Horn EP, Kurz A, Sessler DI: Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med 2000; 342:161–7
Sessler DI, Akca O: Nonpharmacological prevention of surgical wound infections. Clin Infect Dis 2002; 35:1397–404
Greif R, Laciny S, Rapf B, Hickle RS, Sessler DI: Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology 1999; 91:1246–52
Purhonen S, Turunen M, Ruohoaho UM, Niskanen M, Hynynen M: Supplemental oxygen does not reduce the incidence of postoperative nausea and vomiting after ambulatory gynecologic laparoscopy. Anesth Analg 2003; 96:91–6
Jensen AG, Kalman SH, Eintrei C, Fransson SG, Morales O: Atelectasis and oxygenation in major surgery with either propofol with or without nitrous oxide or isoflurane anaesthesia. Anaesthesia 1993; 48:1094–6
Joyce CJ, Baker AB: Effects of inspired gas composition during anaesthesia for abdominal hysterectomy on postoperative lung volumes. Br J Anaesth 1995; 75:417–21
Gunnarsson L, Strandberg A, Brismar B, Tokics L, Lundquist H, Hedenstierna G: Atelectasis and gas exchange impairment during enflurane/nitrous oxide anaesthesia. Acta Anaesthesiol Scand 1989; 33:629–37
Gunnarsson L, Tokics L, Gustavsson H, Hedenstierna G: Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. Br J Anaesth 1991; 66:423–32
Serafini G, Cornara G, Cavalloro F, Mori A, Dore R, Marraro G, Braschi A: Pulmonary atelectasis during paediatric anaesthesia: CT scan evaluation and effect of positive endexpiratory pressure (PEEP). Paediatr Anaesth 1999; 9:225–8
Davis GM, Coates AL, Papageorgiou A, Bureau MA: Direct measurement of static chest wall compliance in animal and human neonates. J Appl Physiol 1988; 65:1093–8
Keens TG, Bryan AC, Levison H, Ianuzzo CD: Developmental pattern of muscle fiber types in human ventilatory muscles. J Appl Physiol 1978; 44:909–13
Craig DB, Wahba WM, Don HF, Couture JG, Becklake MR: “Closing volume” and its relationship to gas exchange in seated and supine positions. J Appl Physiol 1971; 31:717–21
Vaughan RW, Wise L: Intraoperative arterial oxygenation in obese patients. Ann Surg 1976; 184:35–42
Hedenstierna G, Santesson J: Breathing mechanics, dead space and gas exchange in the extremely obese, breathing spontaneously and during anaesthesia with intermittent positive pressure ventilation. Acta Anaesthesiol Scand 1976; 20:248–54
Pelosi P, Croci M, Ravagnan I, Tredici S, Pedoto A, Lissoni A, Gattinoni L: The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998; 87:654–60
Shnider SM, Levinson G: Anesthesia for obstetrics, Anesthesia. Edited by Miller RD. New York, Churchill Livingstone, 1994, pp 2031–76Miller RD
New York
Churchill Livingstone
The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301–8
The Acute Respiratory Distress Syndrome Network
Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, Bruno F, Slutsky AS: Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: A randomized controlled trial. JAMA 1999; 282:54–61
de Durante G, del Turco M, Rustichini L, Cosimini P, Giunta F, Hudson LD, Slutsky AS, Ranieri VM: ARDSNet lower tidal volume ventilatory strategy may generate intrinsic positive end-expiratory pressure in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2002; 165:1271–4
Pontoppidan H, Geffin B, Lowenstein E: Acute respiratory failure in the adult. N Engl J Med 1972; 287:799–806
Mead J, Collier C: Relation of volume history of lungs to respiratory mechanics in anesthetized dogs. J Appl Physiol 1958; 14:669–78
Egbert LD, Laver MB, Bendixen MD: Intermittent deep breaths and compliance during anesthesia in man. Anesthesiology 1963; 24:57–60
Stevenson GW, Tobin M, Horn B, Chen EH, Przybylo HJ, Hall SC, Cote CJ: A comparison of two ventilator systems using an infant lung model. Anesthesiology 2000; 93:285–91
Dueck R, Young I, Clausen J, Wagner PD: Altered distribution of pulmonary ventilation and blood flow following induction of inhalation anesthesia. Anesthesiology 1980; 52:113–25
Gunnarsson L, Tokics L, Lundquist H, Brismar B, Strandberg A, Berg B, Hedenstierna G: Chronic obstructive pulmonary disease and anaesthesia: Formation of atelectasis and gas exchange impairment. Eur Respir J 1991; 4:1106–16
Marshall BE, Wyche MQ Jr: Hypoxemia during and after anesthesia. Anesthesiology 1972; 37:178–209
Moorthy SS, Haselby KA, Caldwell RL, West KW, Albrecht GT, France LW, Powell JC: Transient right-left interatrial shunt during emergence from anesthesia: Demonstration by color flow Doppler mapping. Anesth Analg 1989; 68:820–2
Laver MB, Morgan J, Bendixen HH, Radford EP Jr: Lung volume, compliance, and arterial oxygen tensions during controlled ventilation. J Appl Physiol 1964; 19:725–33
Nunn JF, Bergman NA, Coleman AJ: Factors influencing the arterial oxygen tension during anaesthesia with artificial ventilation. Br J Anaesth 1965; 37:898–914
Pontoppidan H, Geffin B, Lowenstein E: Acute respiratory failure in the adult. N Engl J Med 1972; 287:690–8
Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G: Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82:832–42
Hickman-Davis J, Matalon S: Surfactant protein B deficiency worsens hyperoxic injury to the alveolar epithelium. Am J Respir Cell Mol Biol 1999; 21:449–50
Burton AC, Patel DJ: Effect on pulmonary vascular resistance of inflation of the rabbit lungs. J Appl Physiol 1958; 12:239–46
Simmons DH, Linde CM, Miller JH: Relation of lung volume and pulmonary vascular resistance. Circ Res 1961; 9:465–8
Whittenberger JL, McGregor M, Berglund E, Borst HG: Influence of state of inflation of the lung on pulmonary vascular resistance. J Appl Physiol 1960; 15:878–82
Benumof JL: Mechanism of decreased blood flow to atelectatic lung. J Appl Physiol 1979; 46:1047–8
Barer GR, Howard P, McCurrie JR, Shaw JW: Changes in the pulmonary circulation after bronchial occlusion in anesthetized dogs and cats. Circ Res 1969; 25:747–64
Marshall BE: Importance of hypoxic pulmonary vasoconstriction with atelectasis. Adv Shock Res 1982; 8:1–12
Duggan M, McCaul CL, McNamara PJ, Engelberts D, Ackerley C, Kavanagh BP: Atelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs. Am J Respir Crit Care Med 2003; 167:1633–40
Webb HH, Tierney DF: Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures: Protection by positive end-expiratory pressure. Am Rev Respir Dis 1974; 110:556–65
Sandhar BK, Niblett DJ, Argiras EP, Dunnill MS, Sykes MK: Effects of positive end-expiratory pressure on hyaline membrane formation in a rabbit model of the neonatal respiratory distress syndrome. Intensive Care Med 1988; 14:538–46
Muscedere JG, Mullen JB, Gan K, Slutsky AS: Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994; 149:1327–34
Imai Y, Kawano T, Iwamoto S, Nakagawa S, Takata M, Miyasaka K: Intratracheal anti-tumor necrosis factor-alpha antibody attenuates ventilator-induced lung injury in rabbits. J Appl Physiol 1999; 87:510–5
Kawano T, Mori S, Cybulsky M, Burger R, Ballin A, Cutz E, Bryan AC: Effect of granulocyte depletion in a ventilated surfactant-depleted lung. J Appl Physiol 1987; 62:27–33
Kallet RH, Siobal MS, Alonso JA, Warnecke EL, Katz JA, Marks JD: Lung collapse during low tidal volume ventilation in acute respiratory distress syndrome. Respir Care 2001; 46:49–52
Ploysongsang Y, Schonfeld SA: Mechanism of production of crackles after atelectasis during low-volume breathing. Am Rev Respir Dis 1982; 126:413–5
Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS: Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model. J Clin Invest 1997; 99:944–52
Chiumello D, Pristine G, Slutsky AS: Mechanical ventilation affects local and systemic cytokines in an animal model of acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 160:109–16
Lindberg P, Gunnarsson L, Tokics L, Secher E, Lundquist H, Brismar B, Hedenstierna G: Atelectasis and lung function in the postoperative period. Acta Anaesthesiol Scand 1992; 36:546–53
Eichenberger A, Proietti S, Wicky S, Frascarolo P, Suter M, Spahn DR, Magnusson L: Morbid obesity and postoperative pulmonary atelectasis: An underestimated problem. Anesth Analg 2002; 95:1788–92
Cote CJ, Goldstein EA, Cote MA, Hoaglin DC, Ryan JF: A single-blind study of pulse oximetry in children. Anesthesiology 1988; 68:184–8
Brooks-Brunn JA: Postoperative atelectasis and pneumonia. Heart Lung 1995; 24:94–115
Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP: Critical respiratory events in the postanesthesia care unit: Patient, surgical, and anesthetic factors. Anesthesiology 1994; 81:410–8
Ali J, Weisel RD, Layug AB, Kripke BJ, Hechtman HB: Consequences of postoperative alterations in respiratory mechanics. Am J Surg 1974; 128:376–82
Alexander JI, Parikh RK, Spence AA: Postoperative analgesia and lung function: A comparison of narcotic analgesic regimens. Br J Anaesth 1973; 45:346–52
Meyers JR, Lembeck L, O’Kane H, Baue AE: Changes in functional residual capacity of the lung after operation. Arch Surg 1975; 110:576–83
Wahba RW: Perioperative functional residual capacity. Can J Anaesth 1991; 38:384–400
Ballantyne JC, Carr DB, deFerranti S, Suarez T, Lau J, Chalmers TC, Angelillo IF, Mosteller F: The comparative effects of postoperative analgesic therapies on pulmonary outcome: Cumulative meta-analyses of randomized, controlled trials. Anesth Analg 1998; 86:598–612
Manikian B, Cantineau JP, Bertrand M, Kieffer E, Sartene R, Viars P: Improvement of diaphragmatic function by a thoracic extradural block after upper abdominal surgery. Anesthesiology 1988; 68:379–86
Spence AA, Logan DA: Respiratory effects of extradural nerve block in the postoperative period. Br J Anaesth 1975; 47(suppl):281–3
Jayr C, Thomas H, Rey A, Farhat F, Lasser P, Bourgain JL: Postoperative pulmonary complications: Epidural analgesia using bupivacaine and opioids versus parenteral opioids. Anesthesiology 1993; 78:666–76
Rigg JR, Jamrozik K, Myles PS, Silbert BS, Peyton PJ, Parsons RW, Collins KS: Epidural anaesthesia and analgesia and outcome of major surgery: A randomised trial. Lancet 2002; 359:1276–82
Pizov R, Takahashi M, Hirshman CA, Croxton T: Halothane inhibition of ion transport of the tracheal epithelium: A possible mechanism for anesthetic-induced impairment of mucociliary clearance. Anesthesiology 1992; 76:985–9
O’Callaghan C, Atherton M, Karim K, Gyi A, Langton JA, Zamudio I, Barry P: The effect of halothane on neonatal ciliary beat frequency. J Paediatr Child Health 1994; 30:429–31
Forbes AR, Gamsu G: Depression of lung mucociliary clearance by thiopental and halothane. Anesth Analg 1979; 58:387–9
Konrad F, Schraag S, Marx T, Kilian J, Goertz A: The effect of total intravenous anesthesia with propofol, alfentanil and vecuronium (TIVA) on bronchial mucosal transport [in German]. Anasthesiol Intensivmed Notfallmed Schmerzther 1998; 33:171–6
Cervin A, Lindberg S: Changes in mucociliary activity may be used to investigate the airway-irritating potency of volatile anaesthetics. Br J Anaesth 1998; 80:475–80
Warner DO: Preventing postoperative pulmonary complications: The role of the anesthesiologist. Anesthesiology 2000; 92:1467–72
Griffin SM, Shaw IH, Dresner SM: Early complications after Ivor Lewis subtotal esophagectomy with two-field lymphadenectomy: Risk factors and management. J Am Coll Surg 2002; 194:285–97
Lawrence VA, Hilsenbeck SG, Mulrow CD, Dhanda R, Sapp J, Page CP: Incidence and hospital stay for cardiac and pulmonary complications after abdominal surgery. J Gen Intern Med 1995; 10:671–8
Brooks-Brunn JA: Predictors of postoperative pulmonary complications following abdominal surgery. Chest 1997; 111:564–71
Lam WW, Chen PP, So NM, Metreweli C: Sedation versus general anaesthesia in paediatric patients undergoing chest CT. Acta Radiol 1998; 39:298–300
McCulloch PR, Forkert PG, Froese AB: Lung volume maintenance prevents lung injury during high frequency oscillatory ventilation in surfactant-deficient rabbits. Am Rev Respir Dis 1988; 137:1185–92
Dreyfuss D, Soler P, Basset G, Saumon G: High inflation pressure pulmonary edema: Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137:1159–64
Corbridge TC, Wood LD, Crawford GP, Chudoba MJ, Yanos J, Sznajder JI: Adverse effects of large tidal volume and low PEEP in canine acid aspiration. Am Rev Respir Dis 1990; 142:311–5
Sugiura M, McCulloch PR, Wren S, Dawson RH, Froese AB: Ventilator pattern influences neutrophil influx and activation in atelectasis-prone rabbit lung. J Appl Physiol 1994; 77:1355–65
Eichacker PQ, Gerstenberger EP, Banks SM, Cui X, Natanson C: Meta-analysis of acute lung injury and acute respiratory distress syndrome trials testing low tidal volumes. Am J Respir Crit Care Med 2002; 166:1510–4
Richard JC, Maggiore SM, Jonson B, Mancebo J, Lemaire F, Brochard L: Influence of tidal volume on alveolar recruitment: Respective role of PEEP and a recruitment maneuver. Am J Respir Crit Care Med 2001; 163:1609–13
Parker JC, Hernandez LA, Peevy KJ: Mechanisms of ventilator-induced lung injury. Crit Care Med 1993; 21:131–43
Dreyfuss D, Saumon G: Ventilator-induced lung injury: Lessons from experimental studies. Am J Respir Crit Care Med 1998; 157:294–323
Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, Kairalla RA, Deheinzelin D, Munoz C, Oliveira R, Takagaki TY, Carvalho CR: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338:347–54
Ware LB, Matthay MA: The acute respiratory distress syndrome. N Engl J Med 2000; 342:1334–49
DeCampos KN, Keshavjee S, Slutsky AS, Liu M: Alveolar recruitment prevents rapid-reperfusion-induced injury of lung transplants. J Heart Lung Transplant 1999; 18:1096–102
Veith FJ, Sinha SB, Graves JS, Boley SJ, Dougherty JC: Ischemic tolerance of the lung: The effect of ventilation and inflation. J Thorac Cardiovasc Surg 1971; 61:804–10
Hamvas A, Park CK, Palazzo R, Liptay M, Cooper J, Schuster DP: Modifying pulmonary ischemia-reperfusion injury by altering ventilatory strategies during ischemia. J Appl Physiol 1992; 73:2112–9
Borg T, Modig J: Positive effects of prophylactic ventilator treatment on gas exchange and extravascular lung water in a porcine model of adult respiratory distress syndrome induced by endotoxaemia. Acta Chir Scand 1985; 151:501–8
Askanazi J, Wax SD, Neville JF Jr, Hanson EL, Kane PB, Markarian B, Bredenberg CE, Webb WR: Prevention of pulmonary insufficiency through prophylactic use of PEEP and rapid respiratory rates. J Thorac Cardiovasc Surg 1978; 75:267–72
Simon G: X-ray Diagnosis for Clinical Students. London, Butterworths, 1975, pp 199–201
Prys-Roberts C, Nunn JF, Dobson RH, Robinson RH, Greenbaum R, Harris RS: Radiologically undetectable pulmonary collapse in the supine position. Lancet 1967; 2:399–401
Simon BA: Non-invasive imaging of regional lung function using x-ray computed tomography. J Clin Monit Comput 2000; 16:433–42
Damgaard-Pedersen K, Qvist T: Pediatric pulmonary CT-scanning: Anaesthesia-induced changes. Pediatr Radiol 1980; 9:145–8
Rouby JJ, Puybasset L, Nieszkowska A, Lu Q: Acute respiratory distress syndrome: Lessons from computed tomography of the whole lung. Crit Care Med 2003; 31:S285–95
Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni A: Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158:3–11
Gattinoni L, Pesenti A, Baglioni S, Vitale G, Rivolta M, Pelosi P: Inflammatory pulmonary edema and positive end-expiratory pressure: Correlations between imaging and physiologic studies. J Thorac Imaging 1988; 3:59–64
Rouby JJ: A lung computed tomographic assessment of positive end-expiratory pressure-induced lung overdistension. Am J Respir Crit Care Med 2000; 161:1396–7
Puybasset L, Cluzel P, Gusman P, Grenier P, Preteux F, Rouby JJ: Regional distribution of gas and tissue in acute respiratory distress syndrome: I. Consequences for lung morphology. CT Scan ARDS Study Group. Intensive Care Med 2000; 26:857–69
Dambrosio M, Roupie E, Mollet JJ, Anglade MC, Vasile N, Lemaire F, Brochard L: Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation. Anesthesiology 1997; 87:495–503
Malbouisson LM, Muller JC, Constantin JM, Lu Q, Puybasset L, Rouby JJ: Computed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 163:1444–50
Vieira SR, Puybasset L, Richecoeur J, Lu Q, Cluzel P, Gusman PB, Coriat P, Rouby JJ: A lung computed tomographic assessment of positive end-expiratory pressure-induced lung overdistension. Am J Respir Crit Care Med 1998; 158:1571–7
Adams EW, Counsell SJ, Hajnal JV, Cox PN, Kennea NL, Thornton AS, Bryan AC, Edwards AD: Magnetic resonance imaging of lung water content and distribution in term and preterm infants. Am J Respir Crit Care Med 2002; 166:397–402
Marcucci C, Nyhan D, Simon BA: Distribution of pulmonary ventilation using Xe-enhanced computed tomography in prone and supine dogs. J Appl Physiol 2001; 90:421–30
Edelman RR, Hesselink JR: Clinical Magnetic Resonance Imaging. Philadelphia, WB Saunders, 1990, p 743
WB Saunders
Kim OH, Kim WS, Kim MJ, Jung JY, Suh JH: US in the diagnosis of pediatric chest diseases. Radiographics 2000; 20:653–71
Mann DL, Thompson K, Kaiser J: Cross-sectional echocardiographic characterization of atelectatic lung segments: Differentiation from extracardiac tumors. Chest 1990; 97:404–6
Lichtenstein D, Goldstein I, Mourgeon E, Cluzel P, Grenier P, Rouby JJ: Comparative diagnostic performances of auscultation, chest radiography, and lung ultrasonography in acute respiratory distress syndrome. Anesthesiology 2004; 100:9–15
Lichtenstein DA, Lascols N, Prin S, Meziere G: The “lung pulse”: An early ultrasound sign of complete atelectasis. Intensive Care Med 2003; 29:2187–92
Hubmayr RD: The times are a-changin’: Should we hang up the stethoscope? Anesthesiology 2004; 100:1–2
Dreyfuss D, Basset G, Soler P, Saumon G: Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Respir Dis 1985; 132:880–4
Suter PM, Fairley HB, Isenberg MD: Optimum end-expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 1975; 292:284–9
Grasso S, Mascia L, Del Turco M, Malacarne P, Giunta F, Brochard L, Slutsky AS, Marco Ranieri V: Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002; 96:795–802
Craig DB: Postoperative recovery of pulmonary function. Anesth Analg 1981; 60:46–52
Dohi S, Gold MI: Comparison of two methods of postoperative respiratory care. Chest 1978; 73:592–5
Bartlett RH, Gazzaniga AB, Geraghty TR: Respiratory maneuvers to prevent postoperative pulmonary complications: A critical review. JAMA 1973; 224:1017–21
Hedstrand U, Liw M, Rooth G, Ogren CH: Effect of respiratory physiotherapy on arterial oxygen tension. Acta Anaesthesiol Scand 1978; 22:349–52
Thomas JA, McIntosh JM: Are incentive spirometry, intermittent positive pressure breathing, and deep breathing exercises effective in the prevention of postoperative pulmonary complications after upper abdominal surgery? A systematic overview and meta-analysis. Phys Ther 1994; 74:3–10
Pelosi P, Cereda M, Foti G, Giacomini M, Pesenti A: Alterations of lung and chest wall mechanics in patients with acute lung injury: Effects of positive end-expiratory pressure. Am J Respir Crit Care Med 1995; 152:531–7
Townsend EH Jr, Squire L: Treatment of atelectasis by thoracic traction. Pediatrics 1956; 17:250–7
Michelson RP: Treatment of atelectasis in the newborn by sternal traction. Laryngoscope 1953; 63:379–88
Robbins JJ, Schonberger SH, Jackson SC, Handra D: Successful treatment of postoperative atelectasis by intravenous injection of aminophylline: Report of 4 cases. J Thorac Cardiovasc Surg 1965; 49:874–80
Ranieri VM, Eissa NT, Corbeil C, Chasse M, Braidy J, Matar N, Milic-Emili J: Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1991; 144:544–51
Ito Y, Veldhuizen RA, Yao LJ, McCaig LA, Bartlett AJ, Lewis JF: Ventilation strategies affect surfactant aggregate conversion in acute lung injury. Am J Respir Crit Care Med 1997; 155:493–9
Albert RK, Lakshminarayan S, Hildebrandt J, Kirk W, Butler J: Increased surface tension favors pulmonary edema formation in anesthetized dogs’ lungs. J Clin Invest 1979; 63:1015–8
Taskar V, John J, Evander E, Robertson B, Jonson B: Surfactant dysfunction makes lungs vulnerable to repetitive collapse and reexpansion. Am J Respir Crit Care Med 1997; 155:313–20
Carlton DP, Cummings JJ, Scheerer RG, Poulain FR, Bland RD: Lung overexpansion increases pulmonary microvascular protein permeability in young lambs. J Appl Physiol 1990; 69:577–83
O’Brodovich H, Coates G, Marrin M: Effect of inspiratory resistance and PEEP on 99mTc-DTPA clearance. J Appl Physiol 1986; 60:1461–5
Bshouty Z, Ali J, Younes M: Effect of tidal volume and PEEP on rate of edema formation in in situ perfused canine lobes. J Appl Physiol 1988; 64:1900–7
Zapol WM, Jones R: Vascular components of ARDS: Clinical pulmonary hemodynamics and morphology. Am Rev Respir Dis 1987; 136:471–4
Schindler MB, Bohn DJ, Bryan AC, Cutz E, Rabinovitch M: Increased respiratory system resistance and bronchial smooth muscle hypertrophy in children with acute postoperative pulmonary hypertension. Am J Respir Crit Care Med 1995; 152:1347–52
Rimensberger PC, Cox PN, Frndova H, Bryan AC: The open lung during small tidal volume ventilation: concepts of recruitment and “optimal” positive end-expiratory pressure. Crit Care Med 1999; 27:1946–52