BJA Advance Access originally published online on October 17, 2006
British Journal of Anaesthesia 2006 97(6):883-895; doi:10.1093/bja/ael275
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Quantification of atelectatic lung volumes in two different porcine models of ARDS
1 Department of Anaesthesiology, Johannes Gutenberg-University Mainz, Germany
2 Department of Radiology, Johannes Gutenberg-University Mainz, Germany
*Corresponding author: Department of Anaesthesiology, Johannes Gutenberg-University, Langenbeckstrasse1, D-55101 Mainz, Germany. E-mail: karmrodt{at}uni-mainz.de
Accepted for publication July 31, 2006.
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Abstract |
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Background. Cyclic recruitment during mechanical ventilation contributes to ventilator associated lung injury. Two different pathomechanisms in acute respiratory distress syndrome (ARDS) are currently discussed: alveolar collapse vs persistent flooding of small airways and alveoli. We compare two different ARDS animal models by computed tomography (CT) to describe different recruitment and derecruitment mechanisms at different airway pressures: (i) lavage-ARDS, favouring alveolar collapse by surfactant depletion; and (ii) oleic acid ARDS, favouring alveolar flooding by capillary leakage.
Methods. In 12 pigs [25 (1) kg], ARDS was randomly induced, either by saline lung lavage or oleic acid (OA) injection, and 3 animals served as controls. A respiratory breathhold manoeuvre without spontaneous breathing at different continuous positive airway pressure (CPAP) was applied in random order (CPAP levels of 5, 10, 15, 30, 35 and 50 cm H2O) and spiral-CT scans of the total lung were acquired at each CPAP level (slice thickness=1 mm). In each spiral-CT the volume of total lung parenchyma, tissue, gas, non-aerated, well-aerated, poorly aerated, and over-aerated lung was calculated.
Results. In both ARDS models non-aerated lung volume decreased significantly from CPAP 5 to CPAP 50 [oleic acid lung injury (OAI): 346.9 (80.1) to 96.4 (48.8) ml, P<0.001; lavage-ARDS: 245 17.6) to 42.7 (4.8) ml, P<0.001]. In lavage-ARDS poorly aerated lung volume decreased at higher CPAP levels [232 (45.2) at CPAP 10 to 84 (19.4) ml at CPAP 50, P<0.001] whereas in OAI poorly aerated lung volume did not vary at different airway pressures.
Conclusions. In both ARDS models well-aerated and non-aerated lung volume respond to different CPAP levels in a comparable fashion: Thus, a cyclical alveolar collapse seems to be part of the derecruitment process also in the OA-ARDS. In OA-ARDS, the increase in poorly aerated lung volume reflects the specific initial lesion, that is capillary leakage with interstitial and alveolar oedema.
Keywords: lung, lavage-ARDS; lung, respiratory distress syndrome; measurement techniques, tomography
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Introduction |
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It has recently been hypothesized that the dependent lung in acute respiratory distress syndrome (ARDS) is not collapsed but fluid-filled. This leads to permanent derecruitment of lung parenchyma, that is no cyclic recruitment/derecruitment phenomena occur under positive pressure ventilation.1 2 This is in opposition to the theory that superimposed pressure leads to compression of the dependent lung and finally in the collapse of alveoli by the injured oedematous lung itself.3 Both theories are supported by experimental and diagnostic findings. The ‘flooding theory’ is supported by a parenchymal marker technique (PMT) in an experimental model of oleic acid lung injury (OAI),4 whereas the ‘collapse theory’ is based on computed tomography (CT) studies in experimental lavage-ARDS and in patients.5 6
Both animal models simulate different mechanisms of ARDS: (i) damage of the vascular barrier function; and (ii) dysfunction of the surfactant system. In the injured lung, flooding of alveoli leads to surfactant dysfunction while disruption of the capillary alveolar membrane favours capillary leakage.4 OAI mimics this pathomechanism(s). Oleic acid (OA) injection, into a central vein, produces acute endothelial and alveolar epithelial cell necrosis, resulting in multiple pulmonary microembolism and protein-rich pulmonary oedema in a perfusion distribution-dependent manner.7 8 In contrast, repeated lung lavages with normal saline lead to surfactant depletion but causes little morphological damage to alveolar or perivascular cells.9 10
CT has become a reference tool for evaluation of lung aeration and collapse of lung parenchyma. Spiral-CT allows assessment and quantification of the absolute volume of non-aerated lung by visualizing morphological alterations of the entire lung parenchyma in ARDS.
The aim of this study is to investigate whether the dependent lung is flooded or collapsed in these two different animal models of lung injury. We hypothesized that in the alveolar flooding model the same volume of ‘non-aeration’ will be detected by CT at different airway pressures, whereas in an animal model of alveolar collapse the volume of non-aerated tissue should be markedly reduced at higher airway pressures by alveolar recruitment. A different behaviour of lung recruitment in both animal models would verify two different underlying mechanisms of lung aeration and de-aeration, that is ‘alveolar flooding’ and ‘alveolar collapse’.
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Methods |
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Instrumentation
With state animal care committee approval 15 anaesthetized pigs [25 (1) kg] were investigated in this study. After premedication (azaperone 8 mg kg–1 i.m. and atropine 0.02 mg kg–1 i.m.) anaesthesia was induced by fentanyl 0.01 mg kg–1 (Fentanyl, Janssen Pharmaceuticals, Neuss, Germany) and thiopental 5 mg kg–1 (Trapanal, Fa. Altana Pharma, Konstanz, Germany). To maintain anaesthesia a continuous infusion of thiopental (12–15 mg kg–1 h–1) and boluses of fentanyl (0.1 mg kg–1) were administered i.v. during the entire experiment. The airway was secured by tracheotomy (tracheal tube, ID 9 mm, Ruesch, Kernen, Germany). The animals' lungs were ventilated in pressure-controlled mode with an inspired fraction of oxygen (FIO2) of 0.3 in air, and a positive end-expiratory pressure (PEEP) of 5 cm H2O (Servo 900C; Siemens, Germany). Crystalloids were substituted continuously at a rate of 5 ml kg–1 h–1 (Ringer-solution) i.v. Arterial and venous catheters were inserted for blood pressure monitoring (Sirecust 404-1, Siemens, Germany), blood gas analysis, and drug administration by femoral cut-down. A balloon tipped flow directed pulmonary artery (PA) catheter was introduced into the PA for measurement of PA pressures, pulmonary arterial occlusion pressure (PAOP), and mixed venous blood gas sampling. Typical pressure waveforms obtained by pressure tracings were used to verify the position of all catheters. All intravascular pressures were referenced to the mid-chest level. Airway pressures and flows were assessed by conventional spirometry (S/5 Monitoring, Datex-Ohmeda, Duisburg, Germany). After instrumentation, the animals were transferred to the CT unit and positioned supine.
The animals were randomized into two groups: (i) lavage group: surfactant depletion by repetitive lung lavage with 20 ml kg–1 warmed normal saline.10 Lavages were repeated until a 
/FIO2 ratio <200 was reached after 90 min of intermittent positive pressure ventilation after the last lavage; (ii) oleic acid group: OA (oleic acid, J. T. Baker, Deventer, Holland) was injected in the right atrium (0.09–0.11 ml kg–1 in 20 ml of saline) over 30 min in the supine position. A stable lung injury was defined by /FIO2 ratio <200 for 90 min after OA injection.11 Three animals served as controls, they were anaesthetized, prepared and catheterized according to protocol. None were subjected to experimental lung damage.
If inotropic support was necessary to achieve stable haemodynamics (mean arterial pressure >50 mm Hg) a continuous infusion of epinephrine [3 (2) µg kg–1 h–1] was administered and was maintained at the same rate through the study protocol. After finishing the study protocol, the animals were killed under deep anaesthesia with a bolus of thiopental followed by 40 mval of potassium chloride i.v.
Study protocol
Animals were ventilated via pressure constant ventilation during the whole study protocol: PEEP=5 cm H2O; ventilatory frequency: 10 bpm; FIO2=1.0 and Paw over PEEP to achieve an end tidal carbon dioxide tension (E'CO2) of 5.4 (0.7) kPa. For each spiral-CT acquisition ventilation was interrupted for 30 s during an end-inspiratory breathhold without spontaneous breathing at a predefined sustained continuous positive airway pressure (CPAP). Intermittent positive pressure ventilation was restored to the previous ventilatory parameters immediately after imaging. Parameters were recorded before and after induction of lung injury as follows: heart rate (HR), mean arterial blood pressure (MAP), PAOP, mean pulmonary artery pressure (MPAP), arterial and mixed venous blood samples for shunt calculation with standard formulae. The /FIO2 ratio, and the intrapulmonary shunt proportion (QS/QT) were used to assess the severity of lung injury. A spiral-CT scan of the total lung was achieved at baseline before and after induction of lung injury. In each animal, six different CPAP levels (CPAP level of 5, 10, 15, 30, 35 and 50 cm H2O) were applied for spiral-CT scanning in randomized order.
Lung imaging and image analysis
At each CPAP level, total lung was imaged by a spiral-CT acquisition from the apex to the costophrenic sulcus. Scanning parameters were set to: tube voltage=120 kV, tube current=110 mA, matrix of 512x512 mm, and slice thickness=1 mm (voxel size: 0.34x0.34x1 mm), yielding 160–240 slices at each spiral-CT scan. Scanning time was 30 s (Somatom Plus 4, Siemens, Erlangen, Germany). All images were reconstructed with a high resolution algorithm.
In each CT image, the total lung parenchyma was separated from non-pulmonary tissue (ribs, sternum, spine,heart and diaphragm) by manual segmentation (Software CVViewer, Convis, Germany). Lung segmentation was performed by the same investigator (C.B.). Voxels of every image were distributed into 11 compartments ranging from –1000 to +100 HU (Hounsfield Unit) with a 100 HU-range for each compartment. Total lung volume for each compartment was calculated by multiplication of the voxels size and the total amount of voxels at that respective density range.
For further analysis, the lung was divided into four functional compartments according to HU-attenuation number: Attenuation between –1000 and –900 HU was considered to represent over-aerated lung, attenuation between –900 and –500 HU was considered to represent well-aerated lung, and attenuation between –500 and –100 HU was considered to represent poorly aerated lung. Attenuation between –100 and +100 HU was considered non-aerated lung. The attenuation between –1000 and –100 HU was considered as aerated lung.12
The gas volume was calculated from all voxels with negative HU numbers as: volume of gas (ml)=slice thickness (cm)xpixel area (cm2)xmean attenuation (HU)/–1000 (HU) taking all slices of a spiral-CT scan into account. The tissue volume was obtained by subtracting the gas volume from the total lung volume.13
The cephalocaudal distribution of lung density was analysed by dividing the distance from the apex to the costophrenic sulcus into six equally sized sections (from section #1=costophrenic sulcus to section #6=apex of the lung). The following parameters were calculated for each section: over-aerated, well-aerated, poorly aerated and non-aerated lung.
Statistics
Data are expressed as mean (SD). Differences before and after induction of lung injury were analysed by paired t-test. Differences between different CPAP levels within a group and within sections were calculated using a one-way ANOVA combined with post hoc multiple comparisons by Bonferroni's correction. Differences between both lung injury models were analysed by Mann–Whitney rank sum test. In all test procedures a P<0.05 was considered significant (SigmaStat Version 2.03, SPSS Inc., USA).
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Controls
Three animals served as controls. Haemodynamics, gas exchange values, and CT-based lung volumes are listed in Table 1. Functional lung compartments as measured by different density ranges are shown in Figure 1. The fraction of non-aerated lung volume at CPAP 5 (44.7–67.2 ml) decreased at CPAP 50 (19.5–27 ml). The distribution of non-aerated lung area along the craniocaudal axis showed a decrease of non-aerated lung tissue from the costophrenic sulcus to the apical section and towards the cranial sections at higher CPAP levels as shown in Figure 2.
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, arterial oxygen saturation; 
, standard bicarbonate; Hb, haemoglobinLavage-ARDS
Comparison before and after induction of lung injury
Six animals were studied in the lavage group. The average number of lavages to induce lung injury was 2.8 (0.7). Two animals died of severe hypoxaemia before the entire protocol was completed, thus only five complete data sets (spiral-CT) are available for the CPAP level 10 and four data sets for the CPAP 50.
After induction of lavage-ARDS, the shunt fraction increased from 10.6 (3.5)% to 41.2 (8.2)% (P<0.001) and PaO2 decreased from 72 (5.9) to 16 (5.6) kPa (P<0.001). The arterial 
increased from 4.8 (0.4) to 6.8 (0.2) kPa (P<0.001) which was paralleled by a decrease of the pH from 7.483 (0.039) to 7.326 (0.03) (P<0.001). Dynamic lung compliance decreased from 12.2 (2.8) to 7.4 (2.3) ml mbar–1 (P=0.004). Total lung volume increased from 528 (33.5) to 594.4 (48.7) ml (P=0.022). Tissue volume increased from 64.4 (27.1) to 157.4 (10.9) ml (P<0.001) whereas gas volume decreased from 463.5 (48.7) to 437 (50.4) ml (P=0.017). The non-aerated lung volume increased from 112.6 (45) to 245.1 (17.6) ml (P<0.001). Complete haemodynamics, gas exchange values and CT data before and after induction of lavage-ARDS are shown in Table 2.
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Lung compartments at different CPAP levels
In all animals the total lung volume [594.4 (48.7) ml at CPAP 5 vs 1598.8 (232) ml at CPAP 50, P<0.001] and gas volume [437 (50.4) ml at CPAP 5 vs 1563.2 (226.6) ml at CPAP 50, P<0.001] increased at higher CPAP levels, and the lung tissue volume consequently decreased [157.4 (10) ml at CPAP 5 vs 35.3 (17.3) ml at CPAP 50; P<0.001). The increase of aerated lung volume at higher CPAP levels was caused by an increase of well-aerated and over-aerated lung compartments paralleled by a decrease of non-aerated lung as shown in Figure 3. The volume of non-aerated lung decreased from 245 (17.6) ml at CPAP 5 to 42.7 (4.8) ml at CPAP 50 (P<0.001).
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The distribution of non-aerated lung volume along the craniocaudal axis showed an increase of non-aerated lung tissue from the lung apex to the costophrenic sulcus at each CPAP level as shown in Figure S1 (see Supplementary data online). At each CPAP levels the relative amount of non-aerated lung tissue decreased while well-aerated and over-aerated lung tissue increased within each lung section (Table 3).
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OA-ARDS
Comparison before and after induction of lung injury
Six animals were studied in the OA group, one animal died because of severe hypoxaemia before the protocol was completed. Injection of OA increased shunt fraction from 12.8 (14.6)% to 55.4 (20.1)% (P=0.031). The
decreased from 78 (9.2) to 9.3 (4.6) kPa (P=0.031). PaCO2 increased from 5.5 (1.1) to 10.2 (2.1) kPa (P=0.031) and was accompanied by a decrease in pH from 7.402 (0.09) to 7.134 (0.12) (P=0.031). Dynamic lung compliance decreased from 19.1 (6.9) to 15.4 (7.8) ml bar–1 (P=0.031). The MPAP [12.8 (14.6) mm Hg vs 46.8 (4) mm Hg; P=0.031] and heart rate [104 (25) beats min–1 vs 142 (31) beats min–1; P=0.031] increased. The total lung volume increased from 524.5 (111.4) to 700.2 (185.6) ml (P=0.049) and tissue volume increased from 105 (40.6) to 222.6 (53.3) ml (P=0.022). The volume of non-aerated lung increased from 169.1 (60) to 346.9 (80.1) ml (P=0.019). Complete haemodynamics, gas exchange values and CT data before and after induction of OA-ARDS are listed in Table 4.
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Lung compartments at different CPAP levels
The total lung volume increased from 700.2 (185.6) ml at CPAP 5 to 1586.2 (402) ml at CPAP 50 (P<0.001). Gas volume increased at higher CPAP levels, whereas lung tissue volume decreased. Aerated lung volume increased from CPAP 5 to CPAP 50 (P<0.001), mainly by an increase of the well-aerated and over-aerated lung compartment. Poorly aerated lung volume remained constant for all CPAP levels. Non-aerated lung volume decreased from 346 (80.1) ml at CPAP 5 to 96.4 (48.8) ml at CPAP 50 (P<0.001). All CT data are shown in Figure 4.
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The distribution of non-aerated lung volume along the craniocaudal axis showed an increase of non-aerated lung tissue from the lung apex to the costophrenic sulcus at all CPAP levels. Well-aerated and over-aerated lung volumes increased from the sulcus costophrenicus to the apex within each CPAP level. At increasing CPAP levels the relative amount of non-aerated lung decreased while well-aerated and over-aerated compartments increased within each lung section [Table 5 and Figure S2 (see Supplementary data online)].
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Comparison of both ARDS models
There was no difference between the groups before initiation of lung injury. In OAI higher lung tissue volumes and non-aerated volume was found at CPAP levels of 5, 10 and 15. The volume of poorly aerated lung was higher in the OAI lungs at CPAP of 30, 35 and 50. Complete data comparing the two groups are reported in Table 6.
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Discussion |
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The presence of real alveolar collapse and recruitment within each respiratory cycle vs alveolar flooding in ARDS remains controversial.1 Cyclic collapse and recruitment of lung compartments and overdistension of already opened lung regions by tidal volumes are thought to be significant factors contributing to ventilator-induced lung injury (VILI).14–16 Therefore any experimental evidence for real alveolar collapse will have an important clinical impact in ventilator management in ARDS.
Cyclic collapse and recruitment of lung parenchyma has been visualized by in vivo microscopy,17 dynamic CT18 and electrical impedance tomography19 in lavage-ARDS. On the other hand, constant alveolar flooding throughout the respiratory cycle was shown by the PMT in OAI.20 Thus, it is not clear whether the phenomenon of cyclic collapse and recruitment, is independent of the ARDS-model used. Different mechanisms of aeration and de-aeration may imply different pathomechanisms of VILI. In an animal model of lung collapse the opening pressure is dissipated over a small area, and the lining cells in the vicinity are exposed to large stress.21 In an animal model of alveolar flooding the lung volume subjected to stress is larger, opening pressure is dissipated to a larger area, and the local stress on the lining cells would be smaller. In this scenario, VILI may occur through overdistension of aerated alveoli, rather than shear stress in airways as they open.1 20
In this study, we used two common models of experimental lung injury, simulating early stages of ARDS. Both models are thought to induce different primary lung lesions, namely alveolar flooding induced by OA8 and alveolar collapse by surfactant depletion.10 A thoracic spiral-CT scan of the complete lung was performed, which allows an exact measurement of 3D lung aeration by specific lung densities at different airway pressures (i.e. opening pressures).
Three healthy animals without induction of lung damage served as controls. Non-aerated lung parenchyma was found in the controls predominantly in the caudal sections #1 and #2. Non-aerated lung in the dependent lung is a well-known phenomenon in general anaesthesia and higher FIO2.22–24
In both ARDS groups, the initiation of lung injury caused a significant increase in tissue volume and total lung volume. In lavage-ARDS we expected a decrease in aeration and a reduction of total lung volume as the lung is supposed to collapse under its own weight.25 The increase in total lung volume in our study can be explained by an increased tissue volume, which exceeds the decrease in gas volume. The increase in lung tissue after induction of lavage-ARDS was also reported by others who additionally found that tissue volume remained constant even at increased PEEP levels. This was explained by an excess of extravascular lung water and inflammatory cells.26
In this study the increase in tissue volume could also be the result of not fully retrieving lavage fluid or aggravation of the lung injury over time with development of capillary leakage.27 However, capillary leakage seems unlikely, as with higher CPAP levels tissue volume, non-aerated and poorly aerated lung volumes continuously decreased while the well and over-aerated lung volumes continuously increased. In animals with the same lung injury model and similar weight we found a difference of 46 (8) ml between the installed and the retrieved lavage fluid (3–4% of the total fluid for the lung lavages) in four animals (J. Karmrodt unpublished data). These values are similar to those reported from other investigators.26 28
In the OA-ARDS model, decreased aeration and increased tissue volume were found using spiral-CT.1 27 The significantly higher tissue volume compared with the lavage-ARDS, as a surrogate of lung oedema,13 at low CPAP levels (5–15 cm H2O) may indicate alveolar flooding rather than alveolar collapse. These results are supported by a study in OAI with the PMT, which found an increase in regional lung volume of dependent lung compartments because of alveolar flooding.4 29 However, CT studies showed, that in OAI loss of aeration is caused primarily by lung collapse as a reduction of total lung volume was observed after initiation of OAI.11 30 The results of this study agree with results from PMT and other CT studies1 27 as the total lung and tissue volume increased and well-aerated lung volume decreased. Furthermore, using PMT it was impossible to demonstrate lung opening and collapse during mechanical ventilation.2 20 CT studies, however, characterized OAI by a huge potential for recruitment and derecruitment.30 Whatever mechanism is predominant in OAI, in this study non-aerated lung volume and tissue volume decreased significantly at increased CPAP levels and were paralleled by a recruitment as defined by an increase of well-aerated lung volume.6
The main difference between both lung injury models in this investigation was the fact that in OAI the poorly aerated lung volume did not change when CPAP was increased. In lavage-ARDS, poorly aerated areas decreased at higher CPAP levels which can be explained by the difference in the primary lesion. The pathophysiology of OAI includes inflammatory activation and capillary leakage, extravascular oedema and alveolar flooding. CT studies showed a correlation of extravascular lung water with radiological groundglass-opacity,3 31 which correlate to CT attenuation of poorly aerated lung areas (–100 to –500 HU).32 Our results suggest that there is a certain amount of extravascular lung water (defined by HU) in OAI that remains unaffected by the different CPAP levels.
In both ARDS models non-aerated lung regions were inhomogeneously distributed along the cephalocaudal axis, and predominantly located in the dependent lung regions.6 33 As lung injury was induced with the pigs in the supine position, the lavage fluid was primarily guided to dependent lung areas via bronchial airways and gravity. Lung perfusion in OAI is the dominating factor for the onset of initial lesions. As the healthy lung is mainly perfused in dependent parts, the primary lesion was set in this region.34 In addition to the primary lesion in both models the superimposed pressure30 35 by the weight of the heart,36 contributes to lung collapse in the caudal sections #1 and #2.25 There was a decrease of non-aerated lung volume in both models along the craniocaudal axis at higher CPAP levels. With higher CPAP levels the non-aerated lung volume of more cranial sections (#3–#6) decreased whereas the caudal section remained non-aerated until the applied CPAP levels exceeded the superimposed pressure.30 In OAI, CPAP levels >15 cm H2O were necessary to significantly decrease the non-aerated volume in caudal sections #1 and #2 which is in agreement with studies using the PMT.4 In these studies the authors observed that PEEP values of 15 cm H2O were required to transit fluid-filled alveoli to air-filled alveoli.2
Several studies have noted that re-aeration of non-aerated lung volume is associated with a higher risk of over-aeration of primarily not injured and already aerated lung regions.4 37–39 We found an increased volume of over-aerated lung in cranial lung regions and a progressively increasing amount of over-aerated lung regions towards the caudal lung sections at higher CPAP levels in both animal models and in the controls.
Limitations
ARDS in patients is rarely a result of surfactant depletion. Thus the OA ARDS model may be more comparable with primary ARDS in patients. The results of this study cannot be simply extrapolated to human ARDS in which alveolar flooding rather than lung collapse might be the cause of derecruitment. In addition, subjects in this study were ventilated exclusively with 100% oxygen which might have favoured the presence of resorption atelectasis.23
CT has become a reference tool for the evaluation of aeration and collapse of lung parenchyma. As CT measures a density scale proportional to gas tissue distribution, the definition of recruitment is controversial. A decrease in CT numbers does not necessarily reflect real opening of collapsed alveoli, and might be related to decreasing lung oedema. Other limitations in CT include the underestimation of gas volume as a result of partial volume effects,40 slow acquisition times to assess lung volume and density changes resulting from regional re-distribution of pulmonary blood flow. However, these factors are of minor importance as the slice thicknesses of 1 mm minimizes partial volume effects and the airway pressure was maintained constant at predefined pressure levels by inspiratory breatholds at predefined CPAP levels.
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Conclusion |
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In this study, using two different animal models of Acute Lung Injury, we found an alveolar re-aeration by means of a significant decrease in non-aerated lung volumes paralleled by an increase in well-aerated lung volumes with increasing airway pressures. The animal models differed in the absolute amount of poorly aerated lung volume as it remains constant even at higher CPAP levels in OAI, but in lavage-ARDS the lung was completely re-aerated at high CPAP levels. This is caused by a different initial lesion. Independent of the lung injury model, whether the pathomechanism is collapse or flooding, non-aerated lung can be re-aerated within every respirator cycle. Thus, it is likely that cyclic opening and collapse occurs, and emphasizes the importance of this pathomechanism for the progress of ventilator-induced lung injury.
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Supplementary data |
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Figures S1 and S2 can be found as Supplementary data at British Journal of Anaesthesia online.
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Acknowledgments |
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This study was funded by the German Research Foundation (DFG) Grant no. Ma 2398/3. We thank Alexander Schoellkopf for editorial support.
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Footnotes |
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This study contains parts of the doctoral thesis of Christina Hartmann. 
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References |
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