BJA Advance Access originally published online on December 16, 2005
British Journal of Anaesthesia 2006 96(2):156-166; doi:10.1093/bja/aei299
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
REVIEW ARTICLE |
Alveolar recruitment in acute lung injury
Department of Anaesthesia and Critical Care Medicine, University of Freiburg, Hugstetter Strasse 55, 79106 Freiburg, Germany
* Corresponding author. E-mail: Georg.Mols{at}uniklinik-freiburg.de
 |
Abstract |
|---|
 Top Abstract IntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
Alveolar recruitment is one of the primary goals of respiratory care for acute lung injury. It is aimed at improving pulmonary gas exchange and, even more important, at protecting the lungs from ventilator-induced trauma. This review addresses the concept of alveolar recruitment for lung protection in acute lung injury. It provides reasons for why atelectasis and atelectrauma should be avoided; it analyses current and future approaches on how to achieve and preserve alveolar recruitment; and it discusses the possibilities of detecting alveolar recruitment and derecruitment. The latter is of particular clinical relevance because interventions aimed at lung recruitment are often undertaken without simultaneous verification of their effectiveness.
Keywords: lung, damage; lung, mechanics; lung, pathophysiology
|
Introduction |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
Atelectasis describes the state of absent air in alveoli being attributable to their prolonged collapse. By contrast, atelectrauma describes alveolar damage being a result of transient and repeated closure and reopening of alveoli during the respiratory cycle. Alveolar recruitment refers to the opening of collapsed alveoli, derecruitment to the collapse of open alveoli. The term ongoing recruitment describes the state of sustained alveolar recruitment, preventing derecruitment. From a mechanistic point of view, ongoing recruitment is thus the opposite of atelectasis.
It is a commonly held view among intensivists that ongoing alveolar recruitment, with the aim of avoiding atelectasis and atelectrauma, is beneficial in patients with acute lung injury (ALI). This view is based on the results of experimental studies that demonstrated reduced pulmonary oedema and atelectrauma once the lungs are fully recruited at end-expiration.20 87 125 As atelectrauma may cause local and systemic inflammation, bacterial translocation, and gross barotrauma,20 ongoing alveolar recruitment should be of clinical benefit.
However, extrapolation of experimental data to the bedside is hindered because alveoli in experimentally injured lungs are relatively easy to recruit and those in patients' lungs are not. Not surprisingly then, while few clinicians dispute the benefit of alveolar recruitment in general, they debate the optimal means of achieving and maintaining it in clinical practice. The debate centres around how to adjust PEEP, whether or not to use recruitment manoeuvres, on the value of placing the patient in the prone position, and, most important, on the ‘price’, in terms of airway pressure, that should be paid to recruit the lungs. Accordingly, it is the aim of this review to discuss recent experimental and clinical data on alveolar recruitment in ALI, and to assess the feasibility of transferring experimental concepts into clinical practice.
|
Reasons for recruitment |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
More than 30 yr ago, theoretical calculations suggested that alveolar structures are subjected to high shear forces when closed alveoli are adjacent to open ones.77 Even at a comparatively low inflation pressure of 30 cm H2O, shear forces are comparable to a mechanical stress caused by a pressure of 140 cm H2O.77 These calculations implied that, in order to reduce mechanical stress on the alveolar wall, alveoli should be fully recruited (e.g. by PEEP). An early experimental study, showing that PEEP protects against pulmonary oedema caused by high peak airway pressure, received little attention.125 However, by the early 1990s high PEEP and recruitment manoeuvres were advocated in clinical practice to open closed alveoli.61 This therapeutic strategy primarily aimed at lung protection rather than at improvement of oxygenation. Shortly thereafter, the protective effect of PEEP was confirmed experimentally.87
In clinical practice the question arises, whether it is in fact possible and advisable to open all closed alveoli. In the experimental setting, the lungs are rendered susceptible to atelectasis by various interventions (e.g. surfactant removal with a detergent,112 instillation of hydrochloric acid,79 or infusion of endotoxin4 or oleic acid15). In such experimental models, alveolar recruitment by PEEP reduced the tidal change of alveolar volume, lung trauma, inflammation,113 and the influx of neutrophils.85 However, all of these models lack the structural alterations seen in lung tissue. For example, the later stages of Acute Respiratory Distress Syndrome (ARDS) in humans is associated with depletion of cellular material within the alveoli and with fibrosis.5 These structural alterations in human lung injury render some if not all lung areas more difficult to recruit than in experimental lung injury, which mimics more the early stages of ARDS. Thus, the view that the recruited lung is a good lung is almost exclusively based on findings in the experimentally injured lung. In human ARDS, however, there is no conclusive evidence as to whether recruitment is always beneficial, and if so, what ‘price’, in terms of airway pressure, is acceptable for opening up closed alveoli.
In this context, it is important to clarify whether it is atelectasis per se or atelectrauma that is deleterious. There are no clinical and only few experimental data to answer this question. In human ARDS, three types of alveoli can be distinguished:33 (i) Alveoli, which are open throughout the respiratory cycle. These alveoli are predominantly located in the non-dependent lung areas and are especially prone to overdistension. (ii) Alveoli, which are filled with detritus and other cellular material. They are difficult if not impossible to recruit even with very high pressure. (iii) Alveoli, which are closed, at least at end-expiration. They can be recruited but are susceptible to atelectrauma. In isolated lung preparations, atelectasis caused less activation of TNF-
, MIP-2, and IL-6 than atelectrauma.18 Referring to a previous provocative editorial,61 the investigators concluded with some irony ‘Close the lungs and keep them closed.’18 Although the clinical relevance of these experimental findings is unclear, they, nevertheless, tend to support the belief of many clinicians that ‘full recruitment at any price’ is not worth achieving.
In addition to this clinical argument against the use of high airway pressures for opening up closed alveoli, the entire pathophysiological concept of collapse has recently been questioned.73 74 Most scientists and clinicians believe that atelectasis and atelectrauma are caused by collapse as a result of the weight of the heart and the diseased lung itself, and because of abdominal pressure. If the commonly held view of collapse were true, collapse and reopening would be traumatic, and should, therefore, be avoided. However, recent experimental findings suggested that alveoli are not collapsed but filled with fluid and foam.51 73 74 If the fluid and foam hypothesis were correct, the lungs would be injured by overdistension of aerated alveoli rather than by repeated opening of closed ones.51
At present, this controversy is not settled. Both hypotheses are not mutually exclusive. Collapse and fluid- or foam-filled alveoli could co-exist in the same lung in different regions.
Taking into account both, the results of experimental studies and the arguments against the concept of collapse, aiming at ongoing alveolar recruitment in human ALI seems reasonable. Preliminary data suggest that repeated collapse and reopening (atelectrauma) is worse than atelectasis.
|
Current and future clinical concepts for achieving alveolar recruitment |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
Two clinical trials convincingly showed that the ventilatory strategy can influence survival in patients with ALI and ARDS.3 120 While one of them120 was criticized,23 86 and other trials failed to demonstrate differences in outcome,10 11 115 there is general agreement that ventilatory management affects outcome in patients with ARDS or ALI. Today, low tidal volumes are part of protective ventilation to avoid alveolar overdistension. However, while avoiding overdistension, this strategy may cause derecruitment.107 Consequently, when attempting to further improve survival, measures to counterbalance derecruitment are becoming increasingly important.69
PEEP
In the context of alveolar recruitment, PEEP is of special interest. The American ARDS Net study compared ventilatory strategies using high (13.2±3.5 cm H2O) and low (8.3±3.2 cm H2O) PEEP.121 This trial was stopped prematurely because high PEEP failed to improve outcome. Several factors may have contributed to the negative result. First, in both groups arterial oxygenation was used to guide the level of PEEP. However, as arterial oxygenation varies with systemic haemodynamics in ARDS,19 it does not necessarily reflect alveolar recruitment and is, therefore, not the appropriate means of selecting the level of PEEP required for optimal lung protection. Second, although PEEP was statistically different between both groups (P<0.001), it was relatively low in both groups (8.3±3.2 and 13.2±3.5 cm H2O). In a previous study which showed benefit from PEEP, and other measures,3 PEEP levels were higher (around 16 cm H2O). In the American Network study,121 PEEP was probably high enough to improve oxygenation but too low to protect the lung.
Third, the trial was stopped prematurely. Therefore, from a methodological and statistical point of view, the study does not exclude a beneficial effect of PEEP.
Considering all the limitations, this ARDS Network trial does not provide conclusive evidence for or against a protective effect of an appropriately chosen level of PEEP. The experimentally based rationale for the use of ‘high’ PEEP to protect the lungs remains valid, as there is no conclusive evidence to the contrary.
Recruitment manoeuvres
Recruitment manoeuvres have been repeatedly proposed for alveolar recruitment and lung protection.8 9 15 27 40 54 63 98 123 As yet, no prospective randomized trial has demonstrated any benefit of recruitment manoeuvres on survival of patients with ARDS.48 Thus, we can only discuss its pathophysiological rationale. In general, despite the existence of detailed recommendations,54 there is no consensus on the optimal performance of such recruitment manoeuvres. Their effectiveness depends on the experimental model used,123 which questions the applicability of the general concept to clinical practice. In addition, it is unlikely that the side-effects of short-term very high airway pressure (e.g. temporary overdistension) were detected.8 9 15 27 40 63 98 123 Furthermore, experimental evidence suggests that alveoli may collapse within seconds after recruitment manoeuvres if not stabilized with sufficient PEEP.91–93 On the other hand, a clinical study revealed a longer ‘memory’ of lung tissue for recruitment.65
In order to put the findings into proper perspective, it is important to recall that the PEEP level necessary for alveolar stabilization after a recruitment manoeuvre is comparable to that required for alveolar recruitment by PEEP alone (without preceding recruitment manoeuvres).81 In agreement with this finding, recruitment manoeuvres are less effective at higher baseline PEEP levels,26 and insufficient to keep the lung constantly open at lower ones.40 44 Not unexpectedly, recruitment manoeuvres are only effective in the early stages of ARDS (before fibrosis) where recruitment may still be possible.40 However, even in early ARDS, recruitment is not sustained after such a manoeuvre.96
In conclusion, recruitment manoeuvres may often not be necessary, and at times may even be detrimental. Experimental evidence supporting the use of recruitment manoeuvres is much less robust than that for high PEEP. At present, they cannot be considered standard practice in ARDS or ALI.48
Positioning
Prone positioning improves oxygenation in about two-thirds of patients with ALI or ARDS.39 The mechanisms responsible for this improvement are incompletely understood. Prone positioning affects the distribution of both perfusion and ventilation in a complex way. The change in perfusion is partially caused by gravity and the change in ventilation is partially because of recruitment as a result of reduced compression of lung tissue by the heart in the prone position.2
Such recruitment would be expected to result in lung protection and, subsequently, in improved outcome. However, the only multi-centre trial that investigated this aspect of prone positioning failed to detect any benefit on survival.39 The negative result may, however, be related to limitations in study design: (i) Patients in the ‘prone’ group were turned for only around 7 h per day for a total of 10 days and this may have simply been too short a period.76 (ii) The study protocol was not always followed. Several patients were not turned prone because of lack of staff. Other patients, who had been randomized to the supine group, were turned prone because of severe hypoxaemia. Thus, this trial neither proves nor disproves the effectiveness of the prone position. In conclusion, the prone position improves oxygenation in the majority of patients and leads to alveolar recruitment, which should result in lung protection and better outcome. At present, both seem likely, but remain unproven.
Future ventilatory strategies
The measures discussed thus far are related to conventional mechanical ventilation. However, mechanical ventilation is artificial and unphysiological. In addition to causing substantial elevation of the intrathoracic and intrapulmonal pressures, mechanical ventilation delivers uniform breaths. Such uniformity of breaths occurs not only during controlled mechanical ventilation but also during ventilator assisted spontaneous breathing.84 127 Mechanical ventilation is monomorphous but normal respiration is polymorphous, with continuously changing tidal volume, flow rate, and respiratory rate.25 Based on the physiological argument that life-support systems should mimic noisy patterns,116 and in an attempt to mimic spontaneous breath-to-breath variability, the concepts of polymorphous ventilation126 and of fractal ventilation7 64 have been introduced. Both of these biologically variable patterns are conceptually similar and are based on the idea of a mechanical memory effect. Alveolar recruitment achieved by large tidal volumes exceeds the derecruitment by small tidal volumes with the net effect of recruitment, resulting in improved compliance and oxygenation.116 117 Biologically variable ventilation seems to be superior, with respect to oxygenation, shunt, and airway pressures, to controlled mechanical ventilation, even when periodic sighs88 or repetitive recruitment manouevres32 are added to the latter. Polymorphous ventilation could be a means of maintaining alveolar recruitment without increasing mean airway pressure. Although this is a promising concept of ventilatory support, it has not yet been evaluated clinically.90
|
Detection of alveolar recruitment and derecruitment |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
Ideally, each therapeutic intervention aiming at alveolar recruitment should be evaluated for its effectiveness. Unfortunately, and in contrast to other therapeutic interventions in critical care, such as the application of vasopressors, this is difficult to achieve because, at present, there is no method for direct measurement of alveolar recruitment. We have critically evaluated the quality, validity, and practical usefulness of several indicators of alveolar recruitment.
These indicators can be grouped into four categories:
- indicators of lung function, such as pulmonary gas exchange;
- imaging techniques, such as computed tomography, inductive plethysmography;
- static and dynamic respiratory mechanics;
- measurement of intrapulmonary gas volume.
Pulmonary gas exchange
In clinical practice, ventilator settings are often adjusted to achieve predetermined arterial blood gas tensions. This approach is adequate with respect to oxygenation and carbon dioxide removal. After a change in ventilator settings or other intervention, it is tempting to conclude that an improvement in arterial oxygenation reflects alveolar recruitment. While recruitment may, indeed, be the cause for improved oxygenation, an increase in the arterial partial pressure of oxygen may simply reflect the consequences of a change in ventilator settings on haemodynamics.19 An increase in intrathoracic pressure, resulting from, for example, an increase in PEEP, may reduce venous return to the right atrium. The subsequent reduction in right ventricular end-diastolic volume leading to a substantial decrease in cardiac output is well accepted. In contrast, that a decrease in cardiac output may improve the effectiveness of hypoxic pulmonary vasoconstriction is less frequently taken into consideration. Improved arterial oxygenation may thus be the result of improved hypoxic pulmonary vasoconstriction after a decrease in venous return rather than a result of alveolar recruitment.19 This often neglected physiological mechanism is of practical relevance and may explain, why ventilatory strategies based on blood gas analysis have failed to improve outcome.121
Computed tomography
As arterial oxygenation does not appear to identify a protective PEEP level or to necessarily reflect alveolar recruitment, it seems logical to assess the latter directly. Currently, the method of choice is computed tomography. Its use has greatly contributed to our understanding of alveolar recruitment in ARDS,34 36–38 70 71 103 109 and has allowed differentiation between the pulmonary and extra-pulmonary forms of ARDS.35 67 These findings may35 98 or may not104 be relevant for alveolar recruitment by PEEP and other measures. Some argue that in ARDS of pulmonary origin alveolar recruitment seems to be more difficult35 98 and to require higher PEEP levels109 than in non-pulmonary ARDS. In non-pulmonary ARDS, greater structural inhomogeneity predisposes to overdistension of already open alveoli by high airway pressures, including PEEP. Consequently, distinguishing pulmonary from non-pulmonary ARDS may help to decide whether PEEP should be rather high (pulmonary ARDS) or low (non-pulmonary ARDS). Computed tomography may therefore be useful for the initial titration of PEEP.108 However, ongoing changes in lung morphology, patient positioning, and other variables will require continuous re-assessment of the optimal PEEP level. Therefore, while computed tomography is of unquestionable value in the assessment of the patient with ARDS in general, as far as defining an appropriate ventilatory strategy is concerned, its valued is limited to the initial identification of an appropriate PEEP level.
Inductive plethysmography
The practical limitations of computed tomography led to the search for other methods that would image the lung directly in a tomogram. Amongst these methods, inductive plethysmography (or electrical impedance tomography) is the most attractive one. It is a radiation-free, non-invasive imaging technique, which allows bedside assessment of regional lung ventilation,12 and most fascinating, dynamic evaluation of lung status within each breath.17 59 60 68 94 95 Repetitive passage of small alternating electrical currents via a multiple electrode array placed circumferentially on the chest results in potential differences on the body surface. The voltage pattern is analysed and transformed into a two-dimensional tomogram. As an increase in regional pulmonary air content is accompanied by an increase in local electrical impedance and vice versa, the tomogram can be interpreted as reflecting pulmonary gas distribution. Electrical impedance tomography is characterized by high temporal resolution but relatively low spatial resolution. Although inductive plethysmography has been considerably improved over the past years,29 interpretation of the plethysmography signal remains difficult. At present, this methodology is used in the clinical setting only as a research tool in the monitoring of regional lung ventilation.16 28 30 However, future incorporation of inductive plethysmography into commercially available ventilators or monitoring devices may contribute to more effective monitoring of alveolar recruitment.
Respiratory mechanics
Respiratory mechanics are recorded in an attempt to define the optimal tidal volume and its position on the pressure–volume axis of the lung by defining the correct level of PEEP (Fig. 1). The square within the figure depicts the recruitment area where the lung is neither subjected to overdistension nor to atelectrauma. This area can change over time (Fig. 1, dotted square). It is presently unclear whether it is at all possible to define the recruitment area where ventilator-induced trauma is minimal. Nevertheless, the general purpose of recording respiratory mechanics in ALI is to reduce alveolar trauma by avoiding both overdistension and atelectrauma.
|
Static respiratory mechanics
Traditionally, assessment of respiratory mechanics is based on (quasi-)static measurements. As the word static implies, the lungs' movements need to be interrupted during data acquisition in an attempt to distinguish between the respiratory system's elastic and resistive components of impedance. The simplest static measurement is that of the so called two-point compliance, which is obtained by dividing the volume difference by the pressure difference over a breath after end-inspiratory and end-expiratory hold manoeuvres. Because simple static compliance provides little if any information about the lungs' condition and the effects of ventilator settings, many authors favour the recording of the static pressure–volume curve.45 57 75 78 97 99 100 105 111 124 Usually, only the inspiratory part of the pressure–volume curve is recorded, with the expiratory phase is either not recorded or neglected (Fig. 2A, left). The typical sigmoid curve has two points with maximal curvature, which are called lower (LIP) and upper inflection points (UIP). LIP and UIP of the inspiratory curve are used to select the level of PEEP and the peak airway pressure, respectively. They represent the borders of the recruitment area (Fig. 2A, right).
|
This approach has several shortcomings: (i) Recording of the curve is complicated technically. Several (semi-)automatic devices have been suggested to overcome this limitation.55 102 119 However, none of them has gained widespread acceptance in clinical practice. (ii) Construction of the pressure–volume curve requires assessment of the entire volume range from functional residual capacity (FRC) to total lung volume. This may expose the patient to the risks of both derecruitment46 and overdistension. (iii) The inspiratory part of the pressure–volume curve is greatly modified by recruitment.49 50 52 The LIP may thus not represent the end of recruitment but rather its beginning.49 Consequently, the assumed recruitment area is moved to the right (Fig. 2B, right). Furthermore, as PEEP is an expiratory variable, it is inappropriate to use the LIP of the inspiratory pressure–volume curve for selecting PEEP. For this very reason, some authors favour the use of the expiratory part of the static pressure–volume curve (Fig. 2C).1 50 The point of maximum curvature (PMC) is now marked on the expiratory part of the curve, resulting in a different recruitment area. While this appears logical, it does not resolve the most important objection to the use of static respiratory mechanics for setting the ventilator: (iv) The lungs are never in a static condition, either normally or in intensive care. Basing the prediction of the lungs' dynamic behaviour on static measurements seems highly questionable,114 in the way one would never produce a cardiac arrest in order to measure the performance of the heart.53 Because of the limitations of static respiratory measurements, dynamic measurements are receiving increasing attention.58 62 66 72 101
Dynamic respiratory mechanics
At present, dynamic respiratory mechanics can be studied by several methods: (i) The dynostat algorithm is a method for breath-by-breath analysis of the alveolar pressure–volume curve.55 It does not measure resistance but merely assumes identity of inspiratory and expiratory resistance at each iso-volume. (ii) The modulated low flow technique method includes measurement of resistance.118 By sinusoidal modulation of the gas flow, the resistive pressure component can be separated from the elastic one. The method has recently been amended by an expiratory flow modulation manoeuvre.6 (iii) The stress-index records the pressure–time curve during a constant flow single breath at normal tidal volume (Fig. 3).106 The shape of the pressure–time curve reflects predominantly the change of compliance within this breath and is described mathematically using a simple formula that yields a coefficient b. A coefficient of b<1 indicates downward concavity, that is, increasing compliance with increasing volume. If b>1, concavity is upward, indicating decreasing compliance. Constant compliance can be assumed if b=1, when the pressure–time curve is linear. The stress index assumes that resistance is constant (i.e. independent of volume). This, however, cannot be taken for granted.83 Despite this methodological limitation, the stress-index presents a considerable improvement as it focuses on the actual tidal volume. This actual tidal breath (depicted as a schematic pressure–volume loop in Fig. 2D) is positioned between the static inspiratory and expiratory pressure–volume curves. Both represent extreme, artificial lung conditions, which are of minor practical relevance. Dynamic recordings are therefore more relevant for setting the ventilator than data obtained by the previously mentioned methods. It has recently been shown that pulmonary inflammation could be reduced when the ventilator setting was based on the stress index.89 (iv) The slice-method also analyses the intratidal change of compliance and resistance.42 It is based on standard multiple linear regression,122 and, therefore, does not require a respiratory manoeuvre. Standard multiple regression is used to obtain (whole breath) compliance and resistance in modern ventilators and respiratory monitoring devices. In addition to standard multiple linear regression, the slice-method takes into account dynamic intrinsic PEEP21 and the flow-dependent resistance of the tracheal tube.41 43 However, the most relevant modification lies in subdividing the tidal volume into six volume slices before applying the regression analysis. Thus, by obtaining several values of compliance and resistance per breath, volume-dependency of both parameters is derived. The derivation of the compliance–volume diagram from the pressure–volume recording is shown in Figure 4 for two different PEEP levels in an experimental setting. The number of six slices is not obligatory to the method but rather constitutes a compromise between adequate volume resolution and acceptable noise caused by cardiogenic oscillations. It should be kept in mind that the course of compliance is recorded only within the actual tidal breath. The intratidal compliance–volume curve (compare Fig. 4B) is thus part of the larger (unrecorded) total lung compliance–volume curve. Depending on end-expiratory and end-inspiratory volume, several shapes of intratidal compliance could occur (Fig. 5). Compliance could be constant (Fig. 5A), decreasing (Fig. 5C and D), increasing (Fig. 5E and F), or both increasing and decreasing (Fig. 5B). Thus, the shape of the compliance-curve provides information on whether ventilation takes place at rather high or low lung volume. Unlike other techniques, the ventilator settings and pattern need not be changed for analysis. In patients, the slice-method has been used to assess the appropriateness of ventilator settings and the effects of its changes.65 80 In isolated lungs, it was used to assess alveolar recruitment,82 to establish a new ventilatory strategy,47 and to study the effects of ventilator settings on inflammation.56
|
|
|
It should be noted that both the stress index and the slice-method focus on the actual tidal volume (Fig. 2D). In contrast to static approaches, the recruitment area cannot be directly determined. The change of respiratory mechanics within the breath provides information as to whether or not ventilation actually takes place within the recruitment area. The outer static curve is not ‘seen’ by these methods, and the recruitment area could be defined only by manipulation of PEEP and peak airway pressure. On the other hand, ventilator settings could be constantly monitored for lung protection without the need for a special manoeuvre. After several encouraging studies,47 80 82 89 both methods are awaiting their introduction into routine clinical practice.
Intrapulmonary gas volume
As discussed above, respiratory mechanics are rather complex and there is no consensus as to which approach is best suited to find the least traumatic ventilator settings in ALI. Alternatively, the intrapulmonary gas volume can be determined. The measurement of FRC provides information about the amount of lung tissue involved in gas exchange. FRC is defined as the intrapulmonary gas volume at the end of a normal expiration.13 The rationale of FRC-determination is based on the assumption that the higher the FRC the more alveoli are recruited.110 However, as FRC does not allow differentiation between normal aeration and overdistension, it does not provide information as to whether or not tidal ventilation occurs in the recruitment area (Fig. 1). Nevertheless, determination of FRC is very useful when combined with respiratory mechanics. Determination of FRC is not as simple as expected and is not a routine monitoring tool. The ‘gold standard’ of FRC determination in the intensive care setting is the wash-in/wash-out of a tracer gas in a multiple breath procedure. The intrapulmonary nitrogen volume is completely replaced (washed out) over several breaths by the tracer gas. Hence these methods are better known as nitrogen wash-out. FRC determination using nitrogen wash-out works as long as the intrapulmonary gas volume is freely accessible. As this condition is not necessarily met for the whole lung, as a result of trapped air, the volume determined by nitrogen wash-out has been called ‘accessible pulmonary (gas) volume’ instead of FRC.13 The accuracy of FRC determination critically depends on methodological sophistication such as corrections for changes in gas viscosity or sampling delay time compensation,14 22 which gains special importance during partial ventilatory support.128 Simpler bedside methods for FRC determination using the oxygen wash-out technique have been introduced.24 31 Although an easily available bedside method to determine FRC could be of clinical value with respect to monitoring of alveolar recruitment, especially when combined with respiratory mechanical data, FRC measurements have not been evaluated for their usefulness in clinical practice, because of the aforementioned difficulties.
|
Conclusions |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
A large amount of experimental data suggests that alveolar recruitment is beneficial in ALI and ARDS. However, there is no single clinical study that clearly proves the effectiveness of alveolar recruitment for lung protection and survival. While there is no consensus on what constitutes the best level of PEEP for lung protection, it may be higher than that needed for improving or maintaining arterial oxygenation. In the context of this problem, there is growing evidence that PEEP and other ventilatory variables need to be adjusted individually at the bedside. Although arterial oxygenation is the most easily obtained respiratory variable, it is not suited for this purpose because it is affected by haemodynamic changes. In the near future, lung morphology obtained by bedside methods and respiratory mechanics, especially when based on dynamic recording, may enhance our ability to monitor alveolar recruitment, adjust PEEP, and guide the use of other recruitment measures.
|
Acknowledgments |
|---|
We are indebted to Albert Benzing, MD for reviewing the manuscript and a long time of fruitful discussion on the subject in question.
|
References |
|---|
|
TopAbstractIntroductionReasons for recruitmentCurrent and future clinical...Detection of alveolar...ConclusionsReferences |
|---|
1 Albaiceta GM, Taboada F, Parra D, et al. Tomographic study of inflection points of the pressure–volume curve in acute lung injury. Am J Respir Crit Care Med 2004; 170: 1066–72
2 Albert RK, Hubmayr RD. The prone position eliminates compression of the lungs by the heart. Am J Respir Crit Care Med 2000; 161: 1660–5
3 Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338: 347–54
4 Arold SP, Mora R, Lutchen KR, Ingenito EP, Suki B. Variable tidal volume ventilation improves lung mechanics and gas exchange in a rodent model of acute lung injury. Am J Respir Crit Care Med 2002; 165: 366–71
5 Bellingan GJ. The pulmonary physician in critical care - 6: the pathogenesis of ALI/ARDS. Thorax 2002; 57: 540–6
6 Bitzen U, Drefeldt B, Niklason L, Jonson B. Dynamic elastic pressure–volume loops in healthy pigs recorded with inspiratory and expiratory sinusoidal flow modulation: relationship to static pressure–volume loops. Intensive Care Med 2004; 30: 481–8[CrossRef][ISI][Medline]
7 Boker A, Graham RM, Walley KR, et al. Improved arterial oxygenation with biologically variable or fractal ventilation using low tidal volumes in a porcine model of acute respiratory distress syndrome. Am J Respir Crit Care Med 2002; 165: 456–62
8 Bond DM, Froese AB. Volume recruitment maneuvers are less deleterious than persistent low lung volumes in the atelectasis-prone rabbit lung during high-frequency oscillation. Crit Care Med 1993; 21: 402–12[CrossRef][ISI][Medline]
9 Bond DM, McAloon J, Froese AB. Sustained inflations improve respiratory compliance during high-frequency oscillatory ventilation but not during large tidal volume positive-pressure ventilation in rabbits. Crit Care Med 1994; 22: 1269–77[ISI][Medline]
10 Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. Am J Respir Crit Care Med 1998; 158: 1831–8
11 Brower RG, Shanholtz CB, Fessler HE, et al. Prospective, randomized, controlled trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med 1999; 27: 1492–8[CrossRef][ISI][Medline]
12 Brown BH, Barber DC, Seagar AD. Applied potential tomography: possible clinical applications. Clin Phys Physiol Meas 1984; 6: 109–21
13 Brunner JX, Wolff G. Pulmonary Function Indices in Critical Care Patients. New York, Berlin, Heidelberg: Springer, 1988
14 Brunner JX, Wolff G, Cumming G, Langenstein H. Accurate measurement of N2 volumes during N2 washout requires dynamic adjustment of delay time. J Appl Physiol 1985; 59: 1008–12
15 Cakar N, van der Kloot T, Youngblood M, Adams A, Nahum A. Oxygenation response to a recruitment maneuver during supine and prone positions in an oleic acid-induced lung injury model. Am J Respir Crit Care Med 2000; 161: 1949–56
16 Caples SM, Hubmayr RD. Respiratory monitoring tools in the intensive care unit. Curr Opin Crit Care 2003; 9: 230–5[CrossRef][Medline]
17 Carry PY, Baconnier P, Eberhard A, Cotte P, Benchetrit G. Evaluation of respiratory inductive plethysmography. Accuracy for analysis of respiratory waveforms. Chest 1997; 111: 910–5
18 Chu EK, Whitehead T, Slutsky AS. Effects of cyclic opening and closing at low- and high-volume ventilation on bronchoalveolar cytokines. Crit Care Med 2004; 32: 168–74[CrossRef][ISI][Medline]
19 Dantzker DR, Lynch JP, Weg JG. Depression of cardiac output is a mechanism of shunt reduction in the therapy of acute respiratory failure. Chest 1980; 77: 636–42
20 Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998; 157: 294–323
21 Eberhard L, Guttmann J, Wolff G, et al. Intrinsic PEEP monitored in the ventilated ARDS patient with a mathematical method. J Appl Physiol 1992; 73: 479–85
22 Eberhard L, Haberthür C, Fabry B, Guttmann J. Dynamic delay time compensation for sampling capillaries used in respiratory mass spectrometry. Technol Health Care 1999; 7: 243–59[Medline]
23 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: 1510–14
24 Eichler W, Schumacher J, Roth-Isigkeit A, Braun J, Kuppe H, Klotz KF. Automated evaluation of functional residual capacity by oxygen washout. J Clin Monit Comput 2002; 17: 195–201[CrossRef][Medline]
25 Fadel PJ, Barman SM, Phillips SW, Gebber GL. Fractal fluctuations in human respiration. J Appl Physiol 2004; 97: 2056–64
26 Foti G, Cereda M, Sparacino ME, De Marchi L, Villa F, Pesenti A. Effects of periodic lung recruitment maneuvers on gas exchange and respiratory mechanics in mechanically ventilated acute respiratory distress syndrome (ARDS) patients. Intensive Care Med 2000; 26: 501–7[CrossRef][ISI][Medline]
27 Frank JA, McAuley DF, Gutierrez JA, Daniel BM, Dobbs L, Matthay MA. Differential effects of sustained inflation recruitment maneuvers on alveolar epithelial and lung endothelial injury. Crit Care Med 2005; 33: 181–8[CrossRef][ISI][Medline]
28 Frerichs I, Braun P, Dudykevych T, Hahn G, Quintel M. Distribution of ventilation in young and elderly adults determined by electrical impedance tomography. Respir Physiol Neurobiol 2004; 143: 63–75[CrossRef][ISI][Medline]
29 Frerichs I, Hinz J, Herrmann P, et al. Detection of local lung air content by electrical impedance tomography compared with electron beam CT. J Appl Physiol 2002; 93: 660–6
30 Frerichs I, Schiffmann H, Hahn G, Hellige G. Non-invasive radiation-free monitoring of regional lung ventilation in critically ill infants. Intensive Care Med 2001; 27: 1385–94[CrossRef][ISI][Medline]
31 Fretschner R, Deusch H, Weitnauer A, Brunner JX. A simple method to estimate functional residual capacity in mechanically ventilated patients. Intensive Care Med 1993; 19: 372–6[CrossRef][ISI][Medline]
32 Funk DJ, Graham MR, Girling LR, et al. A comparison of biologically variable ventilation to recruitment manoeuvres in a porcine model of acute lung injury. Respir Res 2004; 5: 22[CrossRef][Medline]
33 Gattinoni L, Caironi P, Pelosi P, Goodman LR. What has computed tomography taught us about the Acute Respiratory Distress Syndrome? Am J Respir Crit Care Med 2001; 164: 1701–11
34 Gattinoni L, Mascheroni D, Torresin A, et al. Morphological response to positive end expiratory pressure in acute respiratory failure. Computerized tomography study. Intensive Care Med 1986; 12: 137–42[ISI][Medline]
35 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
36 Gattinoni L, Pesenti A. Computed tomograpy scanning in acute respiratory failure. In: Zapol WM, Lemaire F, eds. Adult Respiratory Distress Syndrome. New York: Marcel Dekker, Inc., 1991; 199–221.
37 Gattinoni L, Pesenti A, Bombino M, et al. Relationship between lung computed tomography density, gas exchange, and PEEP in acute respiratory failure. Anesthesiology 1988; 69: 824–32[ISI][Medline]
38 Gattinoni L PP, Vitale G, Pesenti A, D'Andrea L, Mascheroni D. Body position changes redistribute lung computed tomography density in patients with acute respiratory failure. Anesthesiology 1991; 74: 15–23[ISI][Medline]
39 Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory distress syndrome. N Engl J Med 2001; 345: 568–73
40 Grasso S, Mascia L, del Turco M, et al. Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002; 96: 795–802[CrossRef][ISI][Medline]
41 Guttmann J, Eberhard L, Fabry B, Bertschmann W, Wolff G. Continuous calculation of intratracheal pressure in tracheally intubated patients. Anesthesiology 1993; 79: 503–13[CrossRef][ISI][Medline]
42 Guttmann J, Eberhard L, Fabry B, et al. Determination of volume-dependent respiratory system mechanics in mechanically ventilated patients using the new SLICE method. Technol Health Care 1994; 2: 175–91
43 Guttmann J, Kessler V, Mols G, Hentschel R, Haberthür C, Geiger K. Continuous calculation of intratracheal pressure in the presence of pediatric endotracheal tubes. Crit Care Med 2000; 28: 1018–26[CrossRef][ISI][Medline]
44 Halter JM, Steinberg JM, Schiller HJ, et al. 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
45 Harris RS, Hess DR, Venegas JG. An objective analyis of the pressure–volume curve in the acute respiratory distress syndrome. Am J Respir Crit Care Med 2000; 161: 432–9
46 Henzler D, Mahnken A, Dembinski R, Waskowiak B, Rossaint R, Kuhlen R. Repeated generation of the pulmonary pressure–volume curve may lead to derecruitment in experimental lung injury. Intensive Care Med 2005; 31: 302–10[CrossRef][ISI][Medline]
47 Hermle G, Mols G, Zügel A, et al. Intratidal compliance–volume curve as an alternative basis to adjust positive end-expiratory pressure: a study in isolated perfused rabbit lungs. Crit Care Med 2002; 30: 1589–97[CrossRef][ISI][Medline]
48 Hess DR, Bigatello LM. Lung recruitment: the role of recruitment maneuvers. Respir Care 2002; 47: 308–17[Medline]
49 Hickling KG. The pressure–volume curve is greatly modified by recruitment: a mathematical model of ARDS lungs. Am J Respir Crit Care Med 1998; 158: 194–202
50 Hickling KG. Best compliance during a decremental, but not incremental, positive end-expiratory pressure trial is related to open-lung positive end-expiratory pressure: a mathematical model of acute respiratory distress syndrome lungs. Am J Respir Crit Care Med 2001; 163: 69–78
51 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
52 Jonson B, Richard J-C, Straus C, Mancebo J, Lemaire F, Brochard L. Pressure–volume curves and compliance in acute lung injury: evidence of recruitment above the lower inflection point. Am J Respir Crit Care Med 1999; 159: 1172–8
53 Jonson B, Svantesson C. Elastic pressure–volume curves: what information do they convey? Thorax 1999; 54: 82–7
54 Kacmarek RM, Schwartz DR. Lung recruitment. Respir Care Clin N Am 2000; 6: 597–623[CrossRef][Medline]
55 Karason S, Sondergaard S, Lundin S, Wiklund J, Stenqvist O. A new method for non-invasive, manoeuvre-free determination of ‘static’ pressure–volume curves during dynamic/therapeutic mechanical ventilation. Acta Anaesthesiol Scand 2000; 44: 578–85[ISI][Medline]
56 Kirchner EA, Mols G, Hermle G, et al. Reduced activation of immunomodulatory transcription factors during positive end-expiratory pressure adjustment based on volume-dependent compliance in the isolated perfused rabbit lung. Br J Anaesth 2005; 94: 530–5
57 Kondili E, Prinianakis G, Hoenig S, Chatzakis G, Georgopoulos D. Low flow inflation pressure–time curve in patients with acute respiratory distress syndrome. Intensive Care Med 2000; 26: 1756–63[CrossRef][ISI][Medline]
58 Kugelman A, Keens TG, deLemos R, Durand M. Comparison of dynamic and passive measurements of respiratory mechanics in ventilated newborn infants. Pediatr Pulmonol 1995; 20: 258–64[ISI][Medline]
59 Kunst PWA, Böhm SH, G Vazquez de Anda, et al. Regional pressure volume curves by electrical impedance tomography in a model of lung injury. Crit Care Med 2000; 28: 178–83[CrossRef][ISI][Medline]
60 Kunst PWA, Vazquez de Anda G, Böhm SH, et al. Monitoring of recruitment and derecruitment by electrical impedance tomography in a model of lung injury. Crit Care Med 2000; 28: 3891–5[CrossRef][ISI][Medline]
61 Lachmann B. Open up the lung and keep the lung open. Intensive Care Med 1992; 18: 319–21[CrossRef][ISI][Medline]
62 Lanteri CJ, Kano S, Nicolai T, Sly P. Measurement of dynamic respiratory mechanics in neonatal and pediatric intensive care: the multiple linear regression technique. Pediatr Pulmonol 1995; 19: 29–45[ISI][Medline]
63 Lapinsky SE, Aubin M, Mehta S, Boiteau B, Slutsky AS. Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intensive Care Med 1999; 25: 1297–301[ISI][Medline]
64 Lefevre GR, Kowalski SE, Girling LG, Thiessen DB, Mutch WA. Improved arterial oxygenation after oleic acid lung injury in the pig using a computer-controlled mechanical ventilator. Am J Respir Crit Care Med 1996; 154: 1567–72[Abstract]
65 Lichtwarck-Aschoff M, Guttmann J, Eberhard L, Fabry B, Birle J, Adolph M. Delayed derecruitment after removal of PEEP in patients with acute lung injury. Acta Anaesthesiol Scand 1997; 41: 675–84[ISI][Medline]
66 Lichtwarck-Aschoff M, Kessler V, Sjöstrand UH, et al. Static versus dynamic respiratory mechanics for setting the ventilator. Br J Anaesth 2000; 85: 577–86
67 Lim C-M, Kim EK, Lee JS, et al. Comparison of the response to the prone position between pulmonary and extrapulmonary acute respiratory distress syndrome. Intensive Care Med 2001; 27: 477–85[CrossRef][ISI][Medline]
68 Loube DI, Andrada T, Howard RS. Accuracy of respiratory inductive plethysmography for the diagnosis of upper airway resistance syndrome. Chest 1999; 115: 1333–7
69 Luecke T, Roth H, Joachim A, et al. Effects of end-inspiratory and end-expiratory pressures on alveolar recruitment and derecruitment in saline-washout-induced lung injury—a computed tomography study. Acta Anaesthesiol Scand 2004; 48: 82–92[CrossRef][ISI][Medline]
70 Malbouisson LM, Busch CJ, Puybasset L, et al. Role of the heart in the loss of aeration characterizing lower lobes in acute respiratory distress syndrome. Am J Respir Crit Care Med 2000; 161: 2005–12
71 Malbouisson LM, Muller J-C, Constantin J-M, et al. 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
72 Maltais F, Reissmann H, Navalesi P, et al. Comparison of static and dynamic measurements of intrinsic PEEP in mechanically ventilated patients. Am J Respir Crit Care Med 1994; 150: 1318–24[Abstract]
73 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
74 Martynowicz MA, Walters BJ, Hubmayr RD. Mechanisms of recruitment in oleic acid-injured lungs. J Appl Physiol 2001; 90: 1744–53
75 Matamis D, Lemaire F, Harf A, Brun-Buisson V, Ansquer JC, Atlan G. Total respiratory pressure–volume curves in the adult respiratory distress syndrome. Chest 1984; 86:58–66
76 McAuley DF, Giles S, Fichter H, Perkins GD, Gao F. What is the optimal duration of ventilation in the prone position in acute lung injury and acute respiratory distress syndrome? Intensive Care Med 2002; 28: 414–18[CrossRef][ISI][Medline]
77 Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol 1970; 28: 596–608
78 Mergoni M, Volpi A, Bricchi C, Rossi A. Lower inflection point and recruitment with PEEP in ventilated patients with acute respiratory failure. J Appl Physiol 2001; 91: 441–50
79 Modelska K, Pittet J-F, Folkesson HG, Broaddus VC, Matthay MA. Acid-induced lung injury: protective effect of anti-interleukin-8 pretreatment on alveolar epithelial barrier function in rabbits. Am J Respir Crit Care Med 1999; 160: 1450–6
80 Mols G, Brandes I, Kessler V, et al. Volume-dependent compliance in ARDS: proposal of a new diagnostic concept. Intensive Care Med 1999; 25: 1084–91[CrossRef][ISI][Medline]
81 Mols G, Hermle G, Fries G, et al. Different strategies to keep the lung open: a study in isolated perfused rabbit lungs. Crit Care Med 2002; 30: 1598–604[CrossRef][ISI][Medline]
82 Mols G, Hermle G, Schubert J, et al. Volume-dependent compliance and ventilation-perfusion mismatch in surfactant-depleted isolated rabbit lungs. Crit Care Med 2001; 29: 144–51[CrossRef][ISI][Medline]
83 Mols G, Kessler V, Benzing A, Lichtwarck-Aschoff M, Geiger K, Guttmann J. Is pulmonary resistance constant, within the range of tidal volume ventilation, in patients with ARDS? Br J Anaesth 2001; 86: 176–82
84 Mols G, von Ungern-Sternberg B, Rohr E, Haberthür C, Geiger K, Guttmann J. Respiratory comfort and breathing pattern during volume proportional assist ventilation and pressure support ventilation: a study on volunteers with artificially reduced compliance. Crit Care Med 2000; 28: 1940–6[CrossRef][ISI][Medline]
85 Monkman SL, Andersen CC, Nahminas C, et al. Positive end-expiratory pressure above lower infle