Mechanisms of atelectasis in the perioperative period

Mechanisms of atelectasis in the perioperative period

Best Practice & Research Clinical Anaesthesiology 24 (2010) 157e169 Contents lists available at ScienceDirect Best Practice & Research Clinical Anae...

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Best Practice & Research Clinical Anaesthesiology 24 (2010) 157e169

Contents lists available at ScienceDirect

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Mechanisms of atelectasis in the perioperative period Göran Hedenstierna, MD, PhD, Professor and Head of Research Department a, *, ĆLennart Edmark, MD, DEAA, Senior Consultant b,1 a b

Uppsala University, Dept of Medical Sciences, Clinical Physiology, 751 85 Uppsala, Sweden Dept of Anesthesia and Intensive Care, Västerås Hospital, 721 89 Västerås, Sweden

Keywords: atelectasis anaesthesia oxygen fraction functional residual capacity recruitment of lung tissue

Atelectasis appears in about 90% of all patients who are anaesthetised. Up to 15e20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Atelectasis can persist for several days in the postoperative period. It is likely to be a focus of infection and may contribute to pulmonary complications. A major cause of anaesthesia-induced lung collapse is the use of high oxygen concentration during induction and maintenance of anaesthesia together with the use of anaesthetics that cause loss of muscle tone and fall in functional residual capacity (a common action of almost all anaesthetics). This causes absorption atelectasis behind closed airways. Compression of lung tissue and loss of surfactant or surfactant function are additional potential causes of atelectasis. Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue results in rapid reappearance of atelectasis. If 40% O2 in nitrogen is used for ventilation of the lungs, atelectasis reappears slowly. A postoxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening. However, a combination of oxygenation and airway suctioning will most likely cause new atelectasis. Recruitment at the end of the anaesthesia followed by ventilation with 100% O2 causes new atelectasis before anaesthesia is terminated but not with ventilation with lower fraction of inspired oxygen (FIO2). Thus, recruitment must be followed by ventilation with moderate FIO2. Ó 2010 Elsevier Ltd. All rights reserved.

* Corresponding author. Tel.: þ46 18 611 41 44; Fax: þ46 18 611 41 53. E-mail addresses: [email protected] (G. Hedenstierna), [email protected] (L. Edmark). 1 Tel.: þ46 21 17 30 00. 1521-6896/$ e see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.bpa.2009.12.002

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Occurrence of atelectasis during anaesthesia Atelectasis appears in about 90% of all patients who are anaesthetised1 (Fig. 1). It is seen both during spontaneous breathing and after muscle paralysis and irrespective of whether intravenous or inhalational anaesthetics are used.2 The atelectatic area on a computed tomography (CT) cut near the diaphragm is about 5e6% of the total lung area but can easily exceed 15e20%. It should also be remembered that the amount of tissue that is collapsed is even larger; the atelectatic area comprising mainly lung tissue whereas the aerated lung consists of only 20e40% tissue, the rest being air. Thus, 15e20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Abdominal surgery does not add much to the atelectasis, but it can persist for several days during the postoperative period.3 It is likely to be a focus of infection and may contribute to pulmonary complications.4 It may also be mentioned that after thoracic surgery and cardiopulmonary bypass, more than 50% of the lung can be collapsed even several hours after surgery.5 The amount of atelectasis decreases towards the apex that is mostly fully aerated6 (Fig. 2).

Fig. 1. Transverse CT scans of the chest approximately 1e2 cm cranial of the diaphragm in the waking state (upper panel) and during anesthesia (lower panel). Note the appearance of densities in the dependent lung regions during anesthesia. The large white area in the right hemithorax is the diaphragm that has been moved cranially during anesthesia.

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Fig. 2. Three-dimensional reconstruction of atelectasis in an anesthetized subject. The chest wall is shown in light grey and the atelectasis in dark grey. Note the rather uneven distribution in the dependent regions of the atelectasis that is larger to the left (near the diaphragm) and decreases to the right towards the apex.

Mechanism of atelectasis formation There appear to be at least three potential causes of atelectasis in an anaesthetised subject: 1. 2. 3. 1.

Absorption atelectasis behind closed airways; Compression of lung tissue; and Loss of surfactant or surfactant function. Absorption atelectasis

In an adult subject, the resting lung volume (functional residual capacity, FRC) is reduced by 0.7e0.8 l by changing the body position from upright to supine, and there is a further decrease by 0.4e0.5 l with the induction of general anaesthesia7 (Fig. 3). As a result, the end-expiratory lung volume (FRC) is reduced from approximately 3.5 to 2 l, the latter being close or equal to residual volume. The decrease in FRC appears to be related to loss of respiratory muscle tone, shifting the balance between the elastic

Fig. 3. Influence of age on FRC awake in different body positions (sitting and supine) and during anesthesia (supine). Closing capacity (CC), the lung volume at which airways begin to close during an expiration, is also shown. Note the increase in FRC with increasing age, provided that body height and weight are constant. Note also the decrease in FRC by approximately 0,7e0,8 l when lying down from upright and the further decrease by another 0,4e0,5 l during anesthesia. Closing capacity increases faster with age so that a certain amount of airway closure occurs above FRC in upright position at ages above 65 years and at around 50 years in the supine position. During anesthesia most patients, above 30 years, will suffer from airway closure.

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recoil force of the lung and the outward forces of the chest wall to a lower chest and lung volume. Anaesthesia per se causes a fall in FRC even if the subject is breathing spontaneously,8,9 and the drop in FRC occurs irrespective of whether the anaesthetic is inhaled or given intravenously.2 Muscle paralysis and mechanical ventilation cause no further decrease in FRC. Maintenance of muscle tone, as during ketamine anaesthesia, does not reduce FRC.10 The major effect of the loss of muscle tone and the subsequent fall in FRC is a cranial displacement of the diaphragm with only a minor contribution by decreased transverse area of the thorax.11e13 However, fairly conflicting results have been reported regarding the diaphragm with only a minor displacement of the diaphragm and the anterior part even being shifted caudally.14 The fall in FRC promotes closure of airways in dependent lung regions during expiration with reopening during the succeeding inspiration or, if the fall in FRC is large enough, during the whole respiratory cycle. Gas will be absorbed in alveoli behind the closed or intermittently closed airways eventually leading to collapse. It may be understood that the time it takes to absorb all gas behind the occluded airway depends on the gas composition. There are conflicting results regarding the effect on closing capacity (CC) during anaesthesia. Hedenstierna et al. 15 and Rothen et al.16 found a maintained CC whereas Juno et al.17 found a decrease in CC during anaesthesia, in parallel with the decrease in FRC. Fig. 3 is based on the observations made by the Hedenstierna group. 2. Compression atelectasis Compression of lung tissue to the extent that air or gas is pushed out resulting in lung collapse or atelectasis is the major mechanism in acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), where increased lung weight by oedema causes compression of the more dependent lung regions with the typical distribution of collapse and airlessness that is seen in ALI and ARDS. The ‘superimposed’ pressure or weight18 is thus the cause of atelectasis. Whether this occurs also in an essentially lung-healthy subject can be discussed. However, ‘superimposed weight’ may also include the weight of chest wall and abdomen. There is a correlation between body mass index (BMI) and atelectasis,19 and there appears also to be a correlation between the vertical lung height and atelectasis.20 Morbid obesity is accompanied by increased amount of atelectasis21 (Fig. 4). There is thus the possibility that compression is a mechanism of atelectasis during anaesthesia. However, it must be made clear that distinction between these two components, absorption and compression, is difficult to make and whereas absorption is a convincingly proven mechanism, compression is, so far, not. 3. Surfactant deficiency Surfactant is produced by alveolar type 2 cells and stabilises the alveolus so that a small alveolus with a higher surface tension will not empty into a larger alveolus with a lower surface tension, which would eventually result in one single alveolus. Surfactant may be affected by anaesthesia.22 Furthermore, a lack of intermittent deep breaths, as is usually the case during mechanical ventilation, may result in a decreased content of active forms of alveolar surfactant.23 A decreased function of surfactant results in reduced alveolar stability, may contribute to liquid bridging in the airway lumen and thereby causes airway closure.24 When the alveolus is re-opened by increased airway pressure, for example, by the application of a positive end-expiratory pressure (PEEP) of 10 cmH2O, the alveolus re-collapses as soon as the PEEP is discontinued.25 This takes less than 1 min or as soon as it has been possible to repeat CT scanning. It may then look surprising and even inconsistent when a vital capacity manoeuvre or the inflation of the lung to þ 40 cmH2O causes a stable lung so that ventilation can then continue at low or normal airway pressures without the re-occurrence of atelectasis.26 However, this can be attributed to the observation that a forceful inflation of the lung releases new surfactant and spreads it out on the alveolar surface and the distal airways, and this makes the lung unit stable again. This may suggest that once PEEP would be discontinued it would be preceded by a forceful inflation of the lung, a vital capacity manoeuvre. This will again stabilise the lung and will prevent new atelectasis formation, unless the high inspired oxygen fraction is used (see below).

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Fig. 4. CT in anesthetized obese patients with the cut 1 cm above the diaphragm. A recruitment maneuver (RM) (airway pressure of 55 cm H2O for 10 seconds) þ PEEP of 10 cm H2O reduced atelectasis and this effect was sustained for 20 minutes. RM þ ZEEP caused a reduction of atelectasis, but this effect could not be seen after 20 minutes. PEEP had no effect on the amount of atelectasis. * p < 0.05 vs anesthesia, y p < 0.05 vs PEEP and RM þ ZEEP. PEEP ¼ positive end expiratory pressure, RM ¼ recruitment maneuver, ZEEP ¼ zero end expiratory pressure. From ref 21, with permission by the editor of Anesthesiology.

Modulating factors and other considerations Oxygen and atelectasis The time it takes for a lung unit to collapse has been the subject of theoretical studies. Dantzker et al.27 calculated the influence of inspired alveolar ventilation/perfusion ratio (VAI/Q) and inspired oxygen concentration on alveolar stability. They found a critical VAI/Q (when alveoli eventually collapse) approaching 0.001 during air breathing and that was much higher, about 0.07 while breathing 100% oxygen. They also calculated the minimum time to collapse for units with different VAI/Q ratios at different concentrations of inspired oxygen. As can be expected, the minimum time is much longer during air breathing than during ventilation with oxygen. At a VAI/Q ratio of 0.001, it may take 30 min or more during air breathing but no more than 6 min with an fraction of inspired oxygen (FIO2) of 1.0 (see Fig. 5). It was assumed that blood flow through the unit that eventually collapsed was 2 ml min1 ml1 lung unit. For a homogeneous total lung volume of 2.5 l, this would correspond to a capillary blood flow of 5 l min1, which are reasonable values in an anaesthetised, supine man. However, the collapse that can be seen during anaesthesia is found in the most dependent lung regions where initial alveolar size should be smaller than elsewhere in the lung and where blood flow may be higher than the average value. Thus, it is not unlikely that collapse occurs even faster in dependent lung regions on induction of anaesthesia. Pre-oxygenation The most important component of pre-oxygenation is to build up a large oxygen store in the lungs prior to the induction of anaesthesia to prevent hypoxaemia in the event of a difficult intubation of the airway or a problem with ventilation. For the anaesthetist, it will be an important reason not to avoid

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Fig. 5. Dependence of the critical inspired ventilation-perfusion ratio (VAI/Q) on inspired O2 concentration (from 39 with permission inspired ventilation-perfusion ratios at different inspired oxygen concentrations). The calculations have been made on the assumption that the blood flow has been 2 ml/min/ml lung unit. From ref 27 with permission by the editor of J Appl Physiol.

the pre-oxygenation procedure. However, the formation of atelectasis should be recalled and by itself would shorten the ‘apnoea tolerance time’, that is, the time before hypoxaemia develops, since it causes a shunt that lowers the partial pressure of oxygen (PaO2). As can bee seen in Fig. 6, oxygen saturation as measured by pulse oximetry during induction of anaesthesia will fall rapidly after a couple of minutes of apnoea and will fall down to a saturation of 90% after 7 min if pre-oxygenation has been performed with 100% O2 and 3.5 min after pre-oxygenation with 60% O2.28 These decreases in saturation will be the net effect of decreasing oxygen store in the lung and shunt formation. In clinical practice, avoiding the pre-oxygenation procedure and ventilation with 30% instead of 100% O2 prevents formation of atelectasis during the induction and subsequent anaesthesia.29 In another study, 12 patients were breathing 100% O2 during the induction of anaesthesia, while another 12 were breathing 80% O2 and 12 others breathed 60% O2.28 Atelectasis appeared in all patients on 100% O2 and was much smaller in the 80% O2 group, and almost absent in the 60% O2 group (Fig. 7). These findings clearly emphasise the importance of a standard pre-oxygenation procedure in producing atelectasis.

Fig. 6. Decrease in arterial oxygen saturation, as measured by pulse oximetry during apnea after preceding pre-oxygenation with different inspired oxygen concentrations for 3e4 minutes. Note the fairly stable oxygen saturation for the first 2e4,5 minutes and the rapid decline thereafter. From reference 29 with permission by the editor of Anesthesiology.

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Fig. 7. Influence of oxygen concentration during induction of anesthesia on atelectasis formation. Black symbols show individual patients. 12 patients received 100% O2 during 3e4 minutes before induction, their expired O2 (FETO2) being shown. Another 12 patients were preoxygenated with 80% O2 and still another 12 patients with 60% O2. Note the varying amount of atelectasis and the considerable dependence on inspired oxygen concentration. The open symbol (circle) demonstrates the almost complete absence of atelectasis in 10 patients who were preoxygenated with an inspired oxygen concentration of 30%. Data from references28,29. With permission by the editor of Anesthesiology.

Indeed, the atelectasis during anaesthesia is produced at this early occasion with 100% O2 for preoxygenation and need not increase much more during the subsequent anaesthesia and surgery. Whether this is also true when using a lower oxygen fraction for pre-oxygenation remains to be proven. Nitrous oxide It has been assumed that lung collapse occurs faster during ventilation with nitrous oxide (N2O) in oxygen with a common mixture of 60% N2O and 40% O2, than during ventilation with nitrogen and oxygen with the same proportion of the two gases. However, this is in contrast with clinical findings where anaesthesia with nitrous oxide or nitrogen in oxygen produces atelectasis to the same extent and with the same speed.30 It was assumed in the mathematical models that mixed venous inert gas concentrations remain constant, which might be true in steady-state conditions but not necessarily during induction of anaesthesia when inert gas concentrations in mixed venous blood change rapidly. This forced Joyce and Williams31 to expand their theoretical mathematical model to incorporate compartments of peripheral inert gas exchange. This would enable the kinetics of gas absorption to be studied during the early stage of anaesthesia. Based on the clinical observations of atelectasis formation during anaesthesia, Joyce and Williams used a one-lung model with a homogeneously ventilated lung before induction of anaesthesia and a two-compartment lung model with one ventilated lung unit and one non-ventilated lung unit after induction of anaesthesia.31 Moreover, the ventilated lung compartment was divided into one alveolar gas sub-compartment and one lung tissue sub-compartment to take into account the gases that are dissolved in the tissue. Calculations with this model showed that pre-oxygenation for 3 min had a marked effect on the time to collapse, whereas no real difference was seen between nitrous oxide and nitrogen. Even ventilation with air after the pre-oxygentation period caused collapse of lung units within 20e30 min whereas the time for collapse without pre-oxygenation would be around 6 h. Oxygenation and atelectasis during ongoing anaesthesia Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue resulted in a rapid reappearance of the atelectasis.32 If, by contrast, 40% O2 in nitrogen was used for ventilation of the lungs, atelectasis reappeared slowly, and 40 min after the vital capacity manoeuvre only 20% of the initial atelectasis had reappeared. Thus, ventilation during anaesthesia should be done with a moderate FIO2 (e.g., 0.3e0.4) and be increased only if arterial oxygenation is compromised. Post-oxygenation and atelectasis Another situation where a high oxygen concentration is used is at the end of the anaesthesia. A post-oxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening.33 This is mostly done in combination with airway suctioning to eliminate secretions. However,

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the combination of oxygenation and airway suctioning will most likely cause atelectasis, and there is indeed no other potential manoeuvre that can compete with post-oxygenation and airway suctioning in doing so. Recruitment of collapsed lung The findings of atelectasis during anaesthesia and the possibility to recruit lung tissue with an inflation of the lung has prompted studies on the use of recruitment manoeuvre at the end of the surgery and anaesthesia. Again, the influence of inspired oxygen plays an important role. Thus, recruitment at the end of the anaesthesia followed by ventilation with 100% oxygen (the latter again being common in routine anaesthesia) caused new atelectasis within the 10-min period before anaesthesia was terminated but not if ventilation was with lower FIO2.33 Thus, recruitment must be followed by ventilation with moderate FIO2 and the need for high FIO2 should also be less since atelectasis has been eliminated as well as most of the shunt. Hyperoxia High oxygen concentration in inspired air has been advocated by some groups as a precaution against wound infection in the postoperative period. Administration of 80% O2 during the whole anaesthesia and surgery and for another 2e4 h postoperatively has been shown to reduce wound infection in some studies whereas in one study it was accompanied by such an increase in infection that the study was discontinued prematurely.34e36 Whether perioperative oxygen should be used as protection against wound infection can therefore be discussed and any benefit should be balanced against the risk of developing pulmonary infection in atelectatic regions, known to promote inflammation. Composite effects of oxygen and time There are many modulating factors that influence the amount of atelectasis formation during anaesthesia. The influences of age, inspiratory oxygen fraction during maintenance of anaesthesia, duration of anaesthesia, body position, PEEP and airway closure have been described.9,20,25,38 However, in all these studies, no correlation with atelectasis formation to age, inspiratory oxygen fraction during maintenance of anaesthesia or duration of anaesthesia was seen. In the light of new data concerning the crucial role of the oxygen fraction during pre-oxygenation and induction of anaesthesia, some of the earlier conclusions might be re-interpreted. The critical role of the oxygen fraction during pre-oxygenation and induction of anaesthesia was first demonstrated by Rothen et al.29 In this study, pre-oxygenation with 30% oxygen was not followed by formation of atelectasis as measured with CT after about 15 min of anaesthesia. This was true also for patients with a high BMI, another modulating factor. The findings of Rothen et al. were complemented in a study of Reber et al.37 In this study, the influences of pre-oxygenation per se and the oxygen fraction during induction of anaesthesia per se were investigated. Using 100% oxygen both for pre-oxygenation (3 min) and during induction of anaesthesia (3 min), atelectasis formation was about 5 cm2, 10 min after start of induction. Using air during pre-oxygenation (3 min) and 100% oxygen during induction of anaesthesia (3 min), atelectasis formation was only about 2 cm2. A third group had the same procedure during pre-oxygenation and induction of anaesthesia as the second group, but in the third group the effect of hyper-oxygenation during maintenance of anaesthesia was studied, that is, changing FIO2 from 40% to 100% for 15 min. In this third group, the atelectatic area in the basal regions of the lungs was significantly increased while the amount of area with reduced aeration in the basal regions decreased (Fig. 8). The increase in atelectasis close to the diaphragm was much more pronounced than the increase at the carinal level. A most interesting observation was that the mean amount of poor aeration, that is, densities bordering areas of atelectasis, was unchanged after changing the FIO2. The authors interpreted these findings as a series of events, where poorly aerated regions of the lungs collapsed with 100% oxygen, in congruence with the theoretical studies. Lung tissue with reduced aeration before changing the FIO2 was transformed into poorly aerated regions with 100% oxygen, thus keeping the amount of these regions more or less unchanged. As a consequence, the amount of lung tissue with reduced aeration decreased significantly in the basal regions of the lungs.

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Fig. 8. Upper panel: Atelectasis () as measured 1 cm above the diaphragm after induction of anesthesia with and without preoxygenation. Results are presented in cm2 to enable comparison with data taken from 29 in which subjects were ventilated with 30% oxygen in nitrogen. Error bars indicate the standard error of the mean. Lower panel: Graphic representation of study protocol for the three groups depicted in the upper panel. A: induction of anesthesia. B: tracheal intubation. From reference 37 with permission by the editor of Anaesthesia (still waiting for permission).

All these studies are in accordance with the theoretical calculations presented by Joyce and Williams,31 and taken together, these studies make a strong case for the influence of oxygen as one of the main factors governing the amount of atelectasis formation. The early findings in the work from 198525 can thus be reinterpreted. There was no correlation between atelecatasis formation and duration of anaesthesia, probably because the patients had been pre-oxygenated with 100% oxygen and therefore had developed most of the final atelectasis already after 5 min with little further atelectasis during the following 20 min of anaesthesia with 100% oxygen (or close to 100%). The same explanation can be applied to the conclusion that inspiratory oxygen fraction during maintenance of anaesthesia does not correlate with the amount of atelectasis formation. There will be no difference if two groups of patients are both pre-oxygenated with 100% oxygen before intubation and then ventilated with 40% or 100% oxygen, as the effect of 100% oxygen for pre-oxygenation is such a strong determinant to atelectasis formation. An intriguing and puzzling result that derived from this study25 was the conclusion that the amount of atelectasis during anaesthesia was not correlated to age. This result was reproduced in a later study.1 Increasing amount of airway closure seems to explain the age-dependent fall in oxygenation awake.38 An age-dependent increase in airway closure is seen during anaesthesia as well, reasonably contributing or causing the worsening of ventilation/perfusion matching seen with age1 (Fig. 3). One might then assume that atelectasis during anaesthesia would be age dependent. However, yet another study16 showed no correlation between atelectasis and airway closure during anaesthesia, giving further support to the absence of a relationship between atelectasis and age. However, this conclusion or assumption may not be true. We propose a possible explanation for the lack of finding a relationship between atelectasis formation and age or between airway closure and atelectasis during anaesthesia. In the waking state, arterial oxygenation decreases with age, due to a steadily increasing amount of airway

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closure. Common knowledge has since many years taught us that at an age of 50 years closing volume (CV) might be larger than endexpiratory reserve (ERV) in the supine position, and at 65 years this appears in the upright position as well38 (Fig 3). The increasing amount of airway closure causes not only an impaired ventilation distribution but also a slower nitrogen washout during oxygen breathing (e.g., during pre-oxygenation). It could be hypothesized that this slower nitrogen washout (and oxygen washin) could have an effect during pre-oxygenation, so that older people will need a longer time for equilibration between the fraction of endtidal oxygen (FEO2) and FIO2. Young people however, will quickly reach a FEO2 concentration that is very near to the inspired oxygen concentration, but in older people FEO2 will be lower in the beginning of preoxygenation. Studies on pre-oxygenation has not normally included evaluations of atelectasis formation, but it is reasonable to assume that duration of apnoea without desaturation, as measured in these studies, is mainly a reflection of the oxygen storage in the lung, expressed as FEO2 times the lung volume at end-expiration (FRC). From the studies on atelectasis, we know that the impact of the level of oxygen during pre-oxygenation and thus FEO2 is a key determinant of atelectasis formation. So reducing the time for pure pre-oxygenation will unravel this difference, especially during the first minutes of pre-oxygenation.39,40 Even the technique used for pre-oxygenation can have an influence.39,40 In more diseased states, pre-oxygenation takes a longer time, as, for example, was found in patients with severe diffuse emphysema.41 Thus, Gunnarsson et al.42 investigated 10 patients with chronic obstructive pulmonary disease (COPD) during anaesthesia and found only minor atelectasis, probably due to an unchanged FRC (Fig. 9). However, a lower FEO2 after pre-oxygenation cannot be ruled out and would act as a ‘protective’ mechanism. So if not compensated for, old age or chronic obstructive lung disease by lowering the FEO2 might protect

Fig. 9. CT scans in a patient with severe obstructive lung disease awake and during anesthesia. Note the hyper-inflated lung (large transverse lung area) with no atelectasis awake and also no atelectasis during anesthesia, opposite to the finding in lung healthy subjects.

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from atelectasis but shorten the safe time of apnoea. So far, no study on atelectasis has been reported controlling and compensating for the need for longer pre-oxygenation in correlation to age and airway closure at awakening. This could explain the lack of an age dependency of atelectasis formation, because older people will simply have less oxygen behind occluded airways and this will reduce the tendency for atelectasis.

Practice points The bottom line of anaesthetists’ task is to provide anaesthesia that is safe during the surgical procedure and that does not promote postoperative complications. To enable this, the anaesthetist shall  Induce anaesthesia using pre-oxygenation with high enough FIO2 (0.8e1.0) to ensure a long safety time in the event of a difficult intubation or a problem with the airway;  This can be followed by an early recruitment manoeuvre when the airway pressure is increased to 40 cmH2O for 10 s;  Avoid unnecessarily high oxygen fraction during the anaesthesia and surgical procedure, in most patients FIO2 0.3e0.4 should suffice;  Use PEEP with restriction since it does not improve gas exchange on an average e it shall only be used when an oxygenation problem has appeared and it would presumably be better to use a single recruitment manoeuvre to which a modest PEEP of 7e10 cmH2O might be added;  Post-oxygenation is highly discussable since it promotes atelectasis formation that is carried over to the postoperative period e a recruitment manoeuvre should be considered before extubation.

Research agenda Further research is needed to ensure oxygenation in the complicated anaesthetic surgical procedures, in particular, in  Morbidly obese patients to optimise the balance between an open lung and minimum interference with pulmonary and systemic blood flow;  One-lung ventilation for thoracic surgery to optimise ventilation perfusion matching by keeping the ventilated lung open with the least possible redistribution of blood flow to the non-ventilated lung;  Laparoscopic surgery during pneumoperitoneum e although seemingly efficient in terms of gas exchange, we still have no full understanding of the mechanisms that affect the ventilation/perfusion matching;  Using optimum inspired oxygen concentration during induction of anaesthesia as well as during ongoing surgery and during the wake-up period;  Using spontaneous breathing solely or as part of a ventilatory support to improve aeration of the lung and matching of ventilation and blood flow. Although there is a limited incidence of postoperative pulmonary complications in general surgery (3e5%), mortality is high in those who develop complications. Further analysis should be made of intra-operative anaesthesia-related pulmonary dysfunction and postoperative complications.

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Funding source Supported by the Swedish Research Council 5315 and Swedish HearteLung Fund. Conflict of interest statement None. References 1. Gunnarsson L, Tokics L, Gustavsson H et al. Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. British Journal of Anaesthesia 1991; 66: 423e432. *2. Tokics L, Hedenstierna G, Strandberg A et al. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987; 66: 157e167. 3. Strandberg A, Tokics L, Brismar B et al. Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiologica Scandinavica 1986; 30: 154e158. *4. van Kaam AH, Lachmann RA, Herting E et al. Reducing atelectasis attenuates bacterial growth and translocation in experimental pneumonia. American Journal of Respiratory and Critical Care Medicine 2004; 169: 1046e1053. 5. Tenling A, Hachenberg T, Tyden H et al. 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