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Common Health Topics. Treatment of complications. More Information. Bronchiectasis and Atelectasis. Test your knowledge. Mesothelioma is cancer of the membrane that surrounds the chest wall pleura or abdomen. In the United States, which of the following is the only known cause of mesothelioma? More Content. Blockage of the bronchial tubes is a common cause of atelectasis. Shortness of breath can develop if oxygen levels are low or pneumonia occurs. Treatment may involve making sure deep breathing occurs, relieving airway blockages, or both.
Common causes of atelectasis usually involve one of the following. Did You Know Taking deep breaths after surgery can help prevent atelectasis.
Chest x-ray. Deep breathing and coughing. An affected segment of collapse resembles liver so-called hepatization of the lung. Echogenic bands may be visible as a result of a fluid bronchogram. No reinflation of the lung is seen during inhalation. On using colour-flow Doppler, increased flow signals relative to the liver are seen. Lung ultrasound. There is a large pleural effusion causing underlying lung collapse. These include bronchoscopy, thoracoscopy, and open surgery, but these are often more treatment based than purely for diagnosis.
Prevention of atelectasis is preferable to later treatment to re-open collapsed areas of the lung, but techniques for both are similar and based on the causes of atelectasis. Evidence-based studies on the management of atelectasis are lacking. Prevention of atelectasis begins in the preoperative period by identifying high-risk patients and introducing intensive respiratory therapy of physiotherapy, bronchodilators, cessation of smoking, and antibiotics when indicated, at least 5—7 days before operation for elective surgery.
In the setting of more urgent surgery, outcomes may be improved if the operation can be delayed for preoperative respiratory therapy. Common risk factors include patients with pre-existing lung problems chronic obstructive pulmonary disease, asthma, bronchiectasis , smoking, obesity, advanced age, and sleep apnoea. Baseline X-rays, blood gases, and lung function tests are useful for patients with moderate to severe respiratory and cardiovascular disease who are undergoing more major procedures.
During induction of anaesthesia, application of continuous positive airway pressure CPAP can prevent the formation of atelectasis and can increase the margin of safety for oxygenation before intubation. For example, application of CPAP 10 cm H 2 O in morbidly obese patients is effective for the prevention of atelectasis during induction. Optimal modes of ventilation during anaesthesia are unclear, but it is likely that positive pressure ventilation with PEEP, rather than spontaneous ventilation is preferable in longer procedures in at-risk patients.
Whether it is practical or beneficial to allow some spontaneous breaths in longer cases rather that have a patient fully paralysed is unknown. Overall, ventilation strategies should follow those advocated in critical care see below with limited tidal volumes and peak inspiratory pressures. Recruitment of atelectasis should be attempted if it is suspected clinically or in high-risk patients. Research has shown that recruitment of lung units follows a Gaussian distribution; hence, different units recruit at different pressures, range 10—45 cm H 2 O.
In addition to this critical opening pressure, lung recruitment requires time to allow the delivered gas volume to redistribute. Suggested recruitment manoeuvres include: Higher levels of PEEP are generally not beneficial as the shunt does not improve due to redistribution of blood flow in the lung, and the high intra-thoracic pressure leads to decreased venous return and haemodynamic compromise.
Vital capacity manoeuvre using an inflation pressure of 40 cm H 2 O sustained for 10—15 s. Increasing PEEP to 15 cm H 2 O and then increasing tidal volumes to achieve peak inspiratory pressure of 40 cm H 2 O for 10 breaths before then returning to standard ventilator settings.
Atelectasis is one of the most common pulmonary complications in the postoperative period, although it is often clinically insignificant. The altered compliance of lung tissue, impaired regional ventilation, and retained airway secretions contribute to the development of atelectasis.
Postoperative pain interferes with spontaneous deep breathing and coughing resulting in decreases in FRC, leading to atelectasis. In addition to general measures, a variety of lung expansion exercises may reduce postoperative pulmonary complications in selected patients, including chest physical therapy, deep breathing exercises, incentive spirometry, intermittent positive pressure breathing, and CPAP.
Good postoperative pain control may help to minimize postoperative pulmonary complications by enabling earlier ambulation and improving the patient's ability to take deep breaths. Treatment of atelectasis in critically ill patients differs from anaesthesia in that there is commonly a presence of background ALI or infection. There are numerous strategies to consider when attempting to minimize atelectasis during artificial ventilation in critical care patients. CPAP is useful for the management of spontaneously breathing patients with non-obstructive atelectasis, who are unable to breathe deeply.
The aim is to open up collapsed alveoli to reduce shunt and improve ventilation—perfusion homogeneity, hence reversing hypoxaemia. It is the airway pressure above PEEP that is responsible for alveolar recruitment. PEEP will then prevent recollapse. Patients at risk of ALI should have open-lung techniques instituted to optimize oxygenation. PEEP has a protective role in ALI by attenuating surfactant depletion, and reducing shearing stresses, parenchymal injury, and cytokine release.
Typical recruitment measures used in intensive care include: 10 In general recruitment, measures are well tolerated, although systemic hypotension can occur due to reduced cardiac output when a sustained inflation pressure is used in critically ill patients, this can be reduced by adequate fluid filling pre-recruitment.
Optimal recruitment strategies are unknown. Three consecutive volume-limited breaths per minute with a plateau pressure of 45 cm H 2 O also called sigh. Inspired oxygen concentration has a strong influence on atelectasis. This has been described above for absorption atelectasis. In addition, high concentrations of oxygen used during resuscitation may increase the production of reactive oxygen species and contribute to reperfusion injury.
Muscle tone during artificial ventilation can also affect gas exchange. This can be achieved with airway pressure release ventilation or biphasic positive airway pressure. High-frequency oscillation ventilation HFOV may be considered and facilitates lung inflation and recruitment by maintaining mean airway pressure at a constant elevated level while using a piston to cycle the ventilation rate at several hundred times per minute.
This results in tidal volumes that are smaller than the anatomical dead space of lungs with the potential to reduce volutrauma-related lung injury. HFOV minimizes cyclical alveolar distension and collapse. The mean airway pressure is set at 2—3 cm H 2 O above the mean airway pressure on conventional ventilation usually similar or higher than PEEP but below plateau pressure and increased in increments of 1—2 cm H 2 O until improvement in oxygenation occurs.
Others: A variety of further strategies which may be considered in the management of atelectasis are shown in Table 2. These strategies are more likely to be used in ICUs and are not commonly required or used in theatre. There is no strong evidence to support the application of these techniques and so their use should be preceded by an individual risk—benefit analysis for each patient. Other strategies which may be used in the management of artificial ventilation in patients with atelectasis.
FRC, functional residual capacity. Atelectasis is commonly encountered in the perioperative and critical care settings and may lead to hypoxaemia and respiratory failure. Timely diagnosis and management is crucial for a good outcome. The effects of the reverse Trendelenburg position on respiratory mechanics and blood gases in morbidly obese patients during bariatric surgery. Anesth Analg ; 91 : —5. Lung aeration and pulmonary gas exchange during lumbar epidural anaesthesia and in the lithotomy position in elderly patients.
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Anesth Analg ; 88 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Gas exchange and general anaesthesia.
Atelectasis and general anaesthesia. Measurement of atelectasis. Causes of atelectasis formation during general anaesthesia. Factors influencing atelectasis formation. Importance of atelectasis on patient outcome.
Postoperative pulmonary complications. Prevention of atelectasis formation. New concepts of atelectasis during general anaesthesia. Magnusson , L. Corresponding author. Oxford Academic. Google Scholar. Cite Cite L. Select Format Select format. Gas exchange and general anaesthesia In , Nunn 56 showed that during routine anaesthesia and spontaneous ventilation, gas exchange was altered by shunt and uneven ventilation perfusion ratios. Atelectasis and general anaesthesia Atelectasis was early suspected as a cause of impaired oxygenation during general anaesthesia.
Causes of atelectasis formation during general anaesthesia Pulmonary atelectasis may be caused by a variety of factors, which have been classified into three basic mechanisms. Compression atelectasis The rapid formation of atelectasis on induction of anaesthesia, being detectable as soon as CT scans can be made, and the fast reappearance after discontinuation of PEEP suggested that the atelectasis was caused by compression of lung tissue rather than by resorption of gas behind occluded airways.
Absorption atelectasis Absorption atelectasis can occur by two mechanisms. Factors influencing atelectasis formation Fraction of inspired oxygen High oxygen concentration has often been associated with atelectasis formation. Chronic obstructive pulmonary disease In contrast, patients with chronic obstructive pulmonary disease develop only a small shunt and almost no atelectasis during anaesthesia.
Hypoxaemia during induction of anaesthesia In the UK during the s, three pregnant women died annually during induction of general anaesthesia because of failure to ventilate or intubate.
Postoperative pulmonary complications In studies on postoperative pulmonary complications PPC , atelectasis and pneumonia are often considered together because the changes associated with atelectasis may predispose to pneumonia. Prevention of atelectasis formation A VCM can completely abolish atelectasis that develops after induction of general anaesthesia. Conclusion Atelectasis that develops during general anaesthesia may lead to perioperative pulmonary complications.
Open in new tab Download slide. Br J Anaesth. Anesth Analg. 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. 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.
Hyperinflation of the lungs may make them resist collapse. 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.
One of the first articles examining the effects of atelectasis was by Mead and Collier 99 in They noted that when anesthetized dogs were allowed to breathe spontaneously or were paralyzed and ventilated at tidal volumes of approximately 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. These laboratory findings were translated into the perioperative context with the article by Bendixen et al.
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.
An anatomical basis has been suggested for such atelectasis-associated decreased FRC in the context of general anesthesia see Compression Atelectasis. The pressure—volume characteristics of the lung determine the work of breathing, and ventilatory work may be analyzed by plotting pressure against volume. In many situations, the most striking effect of atelectasis is impairment of systemic oxygenation. This was first identified in the context of general anesthesia 2 where the use of passive hyperinflations reversed the hypoxemia.
Atelectasis can occur as a result of hyperoxia. In this situation, the impaired oxygenation can be expressed in terms of Pao 2. The cause of the impaired oxygenation has been shown, using the multiple inert gas technique, to result from increased mismatch of ventilation with perfusion.
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. 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. 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.
Extensive evidence has established the importance of maintenance of lung volume in the prevention of lung injury. The pivotal publication by Webb and Tierney demonstrated 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.
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.
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. In addition, atelectasis worsened the impairment of compliance induced by high tidal volume. These data suggest that in terms of the most meaningful outcome i. 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.
In addition, we demonstrated that right ventricular dysfunction, possibly secondary to increased pulmonary vascular resistance, occurred in the presence of reduced FRC. 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. For example, atelectasis resolves within 24 h after laparoscopy in nonobese subjects. Some pulmonary complications occur during or immediately after anesthesia—mainly hypoxemia.
In a large study with more than 24, patients, 0. The characteristic postoperative mechanical respiratory abnormality after abdominal or thoracic surgery is a restrictive pattern with severely reduced inspiratory capacity, vital capacity, and FRC. Patients in whom postoperative pulmonary complications develop have a relatively greater reduction of FRC, vital capacity, and Pao 2 than those who do not.
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. Manikian et al. Spence and Logan reported no significant impact of postoperative epidural analgesia on oxygenation when compared with patients receiving systemic morphine, and Jayr et al.
Finally, a recent multicenter randomized trial of 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. Two particular aspects of pulmonary defense mechanisms, coughing and removal of particulate matter, are adversely affected by the changes in lung mechanics and breathing pattern ; 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. Desflurane increased mucociliary activity, and the authors concluded that desflurane is an airway irritating compound.
In a series of adults undergoing elective abdominal surgery, postoperative pulmonary complications occurred in 9. 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. Multiple studies have convincingly demonstrated that recruitment provides effective protection against lung injury that is either induced ,, or aggravated ,,, by mechanical stretch. This may assume increasing importance as the role of tidal volume and plateau pressures in ARDS is debated. Most patients with severe lung injury require supportive mechanical ventilation.
It is clear from multiple laboratory , and clinical 95, studies 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 stretch or other etiologies. 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.
Atelectasis is usually suspected when alterations in lung physiology consistent with the development of atelectasis e. However, confirmation of atelectasis is possible through a variety of means. 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. 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. 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.
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.
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. Since then, atelectasis has been studied extensively. In this study, Lundquist et al. Attenuation values in histograms of the lung and atelectasis were studied using two methods of calculating the atelectatic area.
The extent of the atelectasis in the dependent regions can be reduced by PEEP. The lung in ARDS is characterized by a marked increase in lung tissue and a massive loss of aeration. 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.
The threshold of 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 H 2 O. 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. Although magnetic resonance has several advantages over CT e.
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. However, its role in clinical practice remains to be determined. 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. There are other methods of detecting atelectasis in the preclinical setting, including lung lavage levels of cytokines.
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.
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, — it is important to examine how recruitment may be achieved.
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.
Nunn et al. They found that arterial oxygenation increased when a pressure of 40 cm H 2 O was maintained for 40 s; lower pressures, even with modest levels of PEEP, were not effective. 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.
The third group, receiving the alveolar recruitment strategy, had a significant increase in arterial oxygenation during general anesthesia. 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.
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