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* From the Departments of Anesthesiology and Critical Care Medicine (Drs. Luecke, Meinhardt, and Weiss), University Hospital of Mannheim, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany; Department of Critical Care (Drs. Herrmann and Quintel), University of Goettingen, Goettingen, Germany; and the Department of Ambient, Healthy and Safety (Dr. Pelosi), University of Insubria, Varese, Italy.
Correspondence to: Thomas Luecke, MD, Department of Anesthesiology and Critical Care Medicine, University Hospital of Mannheim, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Theodor-Kutzer Ufer, Mannheim 68167, Germany; e-mail: thomas.luecke{at}anaes.ma.uni-heidelberg.de
Abstract
Objective: To compare two lung injury models (oleic acid [OA] and saline solution washout [SW]) regarding lung morphology, regional inflation, and recruitment during static pressure-volume (PV) curves, and the effects of positive end-expiratory pressure (PEEP) below and above the lower inflection point (Pflex).
Methods: Fourteen adult pigs underwent OA or SW lung injury. Lung volumes were measured using CT. PV curves were obtained with simultaneous CT scanning at lung apex and base. Fractional inflation and recruitment were compared to data on PEEP above and below Pflex.
Results: Severity of lung injury was comparable. At zero PEEP, SW showed an increased amount of edema and poorly aerated lung volume, recruitment during inspiration, and a better oxygenation response with PEEP. Whole-lung PV curves were similar in both models, reflecting changes in alveolar inflation or deflation. On the inspiratory PV limb, recruitment and inflation were on the same line, while there was a substantial difference between deflation and derecruitment on the expiratory limb. PEEP-induced recruitment at lung apex and base was at or above the derecruitment line on the expiratory limb and showed no relationship to the whole-lung expiratory PV curve.
Conclusions: The following conclusions were made: (1) OA and SW models are comparable in mechanics but not in lung injury characteristics; (2) neither inspiratory nor expiratory whole-lung PV curves are useful to select PEEP in order to optimize recruitment; and (3) after recruitment, there is no difference in derecruitment between the models at high PEEP, while more collapse occurs at lower PEEP in the basal sections of SW lungs.
Key Words: CT • lung injury models • oleic acid • recruitment • saline solution washout
Animal models of acute lung injury (ALI) are widely used in order to assess the effects of mechanical ventilation in the injured lung under standardized conditions, knowing that those experimental models of lung injury do not necessarily demonstrate the entire clinical picture of the ARDS. The two models most commonly used are oleic acid (OA) infusion and saline solution washout (SW). While SW, as first described by Lachmann et al,1 is thought to cause ALI due to surfactant loss/inactivation and subsequent collapse of instable alveoli with a significant concomitant fall in compliance, OA lung injury is thought to be primarily due to massive alveolar flooding and liquid movement in airways.23 Prior studies45 compared the two models, focusing on gas exchange and hemodynamics. In addition, the response to positive end-expiratory pressure (PEEP), tidal volume, and a recruitment maneuver was assessed by Van der Kloot and coworkers5 using a plethysmograph in order to measure end-expiratory lung volumes. To our knowledge, however, no study has directly compared gas and tissue volumes or different degrees of aeration at baseline, during pressure-volume (PV) maneuvers and during PEEP set along the PV curve in the two models.
The static PV curve of the respiratory system is a classic physiologic method used to describe the mechanical properties of the respiratory system and has been used for many years to determine the magnitude of pathology in lung injuries such as ALI/ARDS.678 More recently, a renewal of interest in the PV curve has appeared because components of the PV curve, specifically the lower and upper inflection points, have been used in an attempt to reduce ventilator-induced lung injury.910111213 While it has been hypothesized that the lower inflection point (Pflex) is caused by large-scale alveolar recruitment,1415 this interpretation has been challenged based on theoretical,16 experimental,17 and clinical data.1819 In addition, the rationale to set the pressure levels according to the data obtained from the inflation limb of the PV curve has been questioned.202122 It is unclear, however, whether there is a distinct morphologic correlate for these PV relationships or whether different models of lung injury result in different PV relationships. Therefore, the following study was carried out for the following reasons: (1) to describe the specific morphologic changes induced by OA infusion and SW; and (2) to assess the relationships between lung morphology and lung volumes during static (PV) and dynamic (mechanical ventilation with PEEP) maneuvers in the two models. For that reason, static PV curves were generated concomitant with CT scans at lung apex and lung base as initially suggested by O'Keefe et al.23
Materials and Methods
Animals and Instrumentation
The study was approved by the Institutional Review Board for the care of animal subjects (University of Heidelberg, Mannheim, Germany). The care and handling was in accord with National Institutes of Health guidelines for ethical animal research. Fourteen anesthetized domestic pigs (mean weight, 43 ± 4 kg [± SD]) were used for the study. Some of the animals were used for additional studies.2124
The animals were premedicated with azaperon, 6 mg/kg IM. Anesthesia was induced with ketamine, 4 mg/kg IV, using an ear vein. The trachea was isolated and cannulated using a 9-mm inner-diameter cuffed endotracheal jet tube (Hi-Lo Jet; Mallinckrodt Medical; St. Louis, MO). After the airway was secured, an additional 3 mg/kg bolus of ketamine along with 6 mg of pancuronium were administered. Anesthesia and muscle relaxation were maintained by continuous infusion of ketamine (10 mg/kg/h), midazolam (1 mg/kg/h), and pancuronium (0.12 mg/kg/h) throughout the experiment. The animals were put in a supine position and administered mechanical ventilation (Siemens Servo Ventilator 300; Siemens-Elema AB; Solna, Sweden) in the volume-controlled mode with a PEEP of 5 cm H2O, an inspiratory/expiratory ratio of 1:2, and a fraction of inspired oxygen of 1.0. A tidal volume of 12 mL/kg and a respiratory rate of 12 to 14 breaths/min were applied to maintain a PaCO2 value within the range of 40 to 50 mm Hg. Distal tracheal pressure was measured by connecting an air-filled pressure transducer (Novotrans II; Medex; Hilliard, OH) to the lumen ending at the tip of the tube.
Initially, a continuous infusion of lactated Ringer solution at a rate of 2 mL/kg/h was administered and increased up to 4 mL/h as indicated by cardiac filling pressures. Central venous and pulmonary artery pressures were measured using a 7.5F flow-directed thermodilution fiberoptic pulmonary artery catheter (Opticath; Abbott Laboratories; North Chicago, IL). The right carotid artery was cannulated with a 20-gauge catheter (Vygon; Ecouen, France) for blood sampling and arterial pressure monitoring. Continuous ECG monitoring was performed. For hemodynamic monitoring, a monitor (Sirecust 1281; Siemens Medical Electronics; Danvers, MA) and pressure transducers (Novotrans II; Medex) were used. All hemodynamic and ventilatory variables were recorded in 1-min intervals via an interface (digital serial RS-232; MIDAS software package; Mannheim Intensive Care Data Acquisition System [developed by our group]) based on a graphical programming language ("G"; LabVIEW 6.1; National Instruments; Austin, TX). Cardiac output was measured in triplicate using the pulmonary artery. Arterial and mixed venous blood gases were analyzed (ABL300; Radiometer A/S; Copenhagen, Denmark).
Recording of Static PV Curves
Prior to each PV curve, a recruitment maneuver was performed by inflating the lungs with a pressure of 40 cm H2O for 15 s to standardize lung volume history and conditions among the animals. After disconnection from the ventilator for 10 s, allowing complete exhalation to the resting volume of the respiratory system, a calibrated 1.5-L syringe was connected to the endotracheal tube. Static PV curves were obtained by inflating the lungs in 100-mL increments up to 1,400 mL or until a maximum static pressure of 50 cm H2O was reached. The lungs were deflated in an identical way immediately thereafter, and the procedure was stopped when a pressure of 0 cm H2O was reached.
After each volume increment or decrement, a 5-s pause was held to obtain static pressure estimates and to obtain a CT scan at a fixed level at lung apex or base (see below). During recording of the static PV curves, all analog pressure signals were filtered, sampled, conditioned, and passed back to a single plug-in board for acquisition directly to the pressure-controlled memory using a front-end signal conditioning system (SCXI-1000; National Instruments). The analog signals were amplified and stored on a hard disk. No corrections for changes in temperature and humidity or oxygen consumption were made for inflation or deflation volume data due to the absence of reliable data for pigs. Pflex was recorded as the pressure at the intersection between the slopes of the initial flat and subsequently steep and linear portions of the inflation limb. The point of maximum curvature (PMC) was identified as the point of intersection between the slopes of the initial flat and subsequently steep portions of the deflation limb of the PV curve.2526
Lung Imaging and Image Analysis
An electron beam CT scanner (Imatron C-150XP EBCT; Imatron; San Francisco, CA) was used for the study. Volumetric data sets are acquired with the scanner by firing electrons at one of four stationary target rings at a rate of 100 ms per sweep, together with continuous table motion up to 30 mm/s. Image reconstruction allows averaging of up to 20 sweeps, resulting in an effective exposure time up to 200 ms (1,240 mA). For CT scanning of the whole lung, the ventilator was switched to the pressure-control mode. The pressure level was set at 40 cm H2O, and the PEEP level was set at zero. Prior to each scan, a recruitment maneuver was performed as described above. After an initial scout image, scans of the whole lungs were performed within 14 to 17 s during end-expiratory hold at zero PEEP and during end-inspiratory hold at 40 cm H2O (collimation, 3 mm; table feed, 4 to 5 mm; reconstruction interval, 2 to 2.5 mm; scan length, 28 to 35 cm; 130 kilovolts; 128 mA; exposure time, 200 ms per image). For PV curves and imaging at different levels of PEEP, single-slice scanning was performed at two discrete anatomic locations: lung apex and lung base. For single-slice scanning after each 100-mL volume step during recording of the PV curves and for the different levels of PEEP, the following parameters were used: collimation, 3 mm; 130 kilovolts; exposure time, 100 ms per image.
Image Analysis
The original 16-bit cross-sectional digital imaging and communication in medicine images were processed and analyzed using the custom-made software package (MALUNA; Mannheim Lung Analyzing Tool [developed by our group]) based on graphical programming language ("G", LabVIEW 6.1, ImaqVision; National Instruments) as described previously.21 Using a manual tracing by eye of the anatomic structures, the images were divided into square pixels (size, 0.46 mm2) and the Hounsfield attenuation of each pixel was computed. After multiplying the square pixels with the slice thickness, the total lung volume of each slice was divided into voxels (volume, 1.84 mm3). Voxels were distributed into 100 compartments ranging from – 1,000 to + 300 Hounsfield units (HU) with a 13-HU range for the corresponding voxels. Total lung volume for each slice was obtained by adding the lung volume of each compartment. As the mean CT number of a given lung volume correlates with the respective proportion of gas and tissue within this lung volume, gas and tissue volumes can be calculated. In a first step, the volume of gas and tissue for each compartment of 13 HU was computed as follows: gas volume = volume xCT/– 1,000; and tissue volume = volume x (1 – CT/– 1,000), where CT is the mean CT number of the compartment analyzed. In a second step, the volume of gas and volume of tissue for the whole lung were calculated by adding the values of the volumes of gas and the volumes of tissue obtained for each compartment of 13 HU.21
The entire lung was divided into four areas of aeration according to its HU attenuation: pulmonary parenchyma having densities ranging from – 1,000 to – 900 HU were classified as overinflated, – 900 to – 500 HU were classified as normally aerated, – 500 to – 100 HU were classified as poorly aerated, and – 100 to + 300 HU were classified as nonaerated (atelectatic).21 Fractional inflation, recruitment, and overinflation were calculated as follows: (1) fractional inflation (percent) = (slice gas volume at x – slice gas volume at 0 mL)/(slice gas volume at 1,400 mL – slice gas volume at 0 mL); (2) fractional recruitment (percent) = (nonaerated lung volume at 0 mL – nonaerated lung volume at x)/(nonaerated lung volume at 0 mL – nonaerated lung volume at 1,400 mL); (3) fractional overinflation (percent) = (overinflated lung volume at x – overinflated lung volume at 0 mL)/(overinflated lung volume at 1,400 mL – overinflated lung volume at 0 mL).
Experimental Protocol
After randomization into the SW or OA-induced lung injury groups, the pigs were intubated and placed supine in the CT scanner. Once instrumentation had been completed and an initial recruitment maneuver had been performed, baseline values were obtained. A static PV curve was performed as described above. SW injury was produced by bilateral lung lavage. The endotracheal tube was disconnected from the ventilator, and warmed saline solution was instilled from a height of 50 cm until a meniscus was seen in the tube. The fluid was retrieved via gravity drainage after 45 s of apnea followed by endotracheal suctioning. Instilled and retrieved volumes were measured. Between the lavages, the pigs received manual ventilation with a fraction of inspired oxygen of 1 using a self-inflating bag (AMBU; AMBU Inc.; Linthicum, MD). The lavage process was repeated until adequate impairment of gas exchange (defined as PaO2 < 200 mm Hg 15 min following the last lavage) was achieved. OA lung injury was induced by injection of 0.15 mL/kg of OA (Mallinckrodt Specialty Chemical; Paris, KY) added to 15 mL of saline solution into the right atrium over a 20-min period. Subsequently, lung injury was established by ventilating the pigs in both groups with a low end-expiratory pressure of 5 cm H2O for 60 min.
Thereafter, another set of measurements (injury) was obtained. A recruitment maneuver was performed and CT scans of the entire lungs were obtained at end-expiration and end-inspiration (pressure level of 40 cm H2O) as described above. Appropriate levels for apex and base scans were identified from the end-expiratory scan and used for single-slice scanning. After another recruitment maneuver, a PV curve along with single-slice scanning at the lung base for each volume step was performed as described above. Pflex was determined from the tracheal pressure curve. The recruitment maneuver was repeated, and a corresponding PV curve along with CT scans at the apex of the lung was performed. Again, Pflex was determined and the mean value of Pflex was calculated. Conventional mechanical ventilation was resumed with PEEP set at 0.5 times Pflex and increased to 1.5 times Pflex and 2 times Pflex in 30-min intervals. Before each increment in PEEP, a set of single-slice CT scans at lung apex and base was obtained during a brief end-expiratory hold, along with a complete set hemodynamic and respiratory measurements. On completion of the study, all animals were killed by a bolus dose of thiopental and potassium chloride.
Statistical Analysis
All values are reported as mean ± SD unless otherwise specified. Two-way analysis of variance for repeated measurements followed by multiple comparisons (Bonferroni) were used to compare both groups (group factor) and the effects of end-expiratory pressure levels (PEEP factor) and interaction after injury (baseline data were excluded from comparison). Individual comparisons between different groups at different PEEP levels were performed with unpaired Student t test. Baseline data between groups were compared using Student t test. Statistical software (SAS 6.12; SAS Institute; Cary, NC) was used for analysis, and p = 0.05 was considered statistically significant.
Results
Baseline Characteristics
There were no differences in hemodynamics, gas exchange, and respiratory parameters at baseline between groups (Tables 1, 2
). Static PV curves before lung injury showed no clear lower or upper inflection points, only minimal hysteresis, and were almost identical for both groups (Fig 1
, left).
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Total Lung Volumes:
Table 3
shows lung volumes for SW and OA-injured lungs. After SW, total resting lung volume at end-expiration (zero PEEP) did not change (1,491 ± 181 mL at baseline vs 1,263 ± 246 mL after SW). While the volume of gas sharply decreased (1,015 ± 266 mL at baseline vs 364 ± 102 mL after SW, p < 0.05), the increase in tissue volume (476 ± 87 mL at baseline vs 926 ± 153 mL after SW, p < 0.05) compensated for the loss of gas, keeping total volume constant. In contrast, total end-expiratory lung volume decreased after OA infusion (1,251 ± 341 mL at baseline vs 964 ± 175 mL after OA, p < 0.05). OA infusion also resulted in a decrease in gas volume (790 ± 303 mL at baseline vs 367 ± 147 mL after OA, p < 0.05) and an increase in tissue volume (461 ± 80 mL at baseline vs 588 ± 119 mL after OA, p < 0.05). Of note, this increase in tissue volume was significantly less than that observed after SW (p < 0.05). While nonaerated lung volumes were comparable (SW, 312 ± 125 mL; OA, 235 ± 106 mL), poorly aerated lung volumes were significantly higher after lung lavage (SW, 722 ± 127 mL; OA, 330 ± 51 mL; p < 0.05). Total lung and gas volumes during end-inspiratory hold at peak airway pressure of 40 cm H2O were comparable between the two groups. Recruited volume was higher in SW compared to OA-injured lungs (SW, 177 ± 147 mL; OA, 94 ± 67 mL; p = 0.05, t test). When changes in nonaerated and poorly aerated lung volumes were added, the decrease was significantly higher in SW lungs (
nonpoor SW, 534 ± 238 mL; OA, 154 ± 77 mL; p = 0.003). End-inspiratory overinflated lung volumes were small after injury compared to baseline (SW, 10 ± 8 mL vs 193 ± 91 mL; OA, 47 ± 13 mL vs 101 ± 79 mL).
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Static pressure-slice volume curves at lung apex and lung base are shown in Figures 2, 3 . For the inflation limb, inflation and recruitment curves were nearly identical for both models of injury and both anatomic locations examined (Fig 2, 3). The pressures at the Pflex, calculated from the fractional inflation and recruitment curves, were comparable to that observed for the whole-lung PV curves (Fig 1, right). Recruitment occurred throughout the entire inflation limb and paralleled inflation. At Pflex in SW lungs, fractional recruitment equaled 18 ± 4% at lung base and 26 ± 5% at lung apex. In OA-injured lungs, values were comparable (22 ± 6% at lung base and 30 ± 6% at lung apex).
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Response to Ventilation With PEEP
The cardiorespiratory effects of PEEP set below and above the Pflex (0.5, 1.5, and 2 times Pflex) are shown in Tables 1and 2. Response to PEEP was more pronounced in SW lungs. In that group, increasing PEEP to 0.5 times Pflex already increased PaO2 to 355 ± 38 mm Hg, compared to 188 ± 35 mm Hg in the OA group (p < 0.05). A further increase in PEEP to 1.5 times Pflex markedly increased PaO2 in both groups (SW, 542 ± 33 mm Hg; OA, 384 ± 42; p < 0.05; compared to 0.5 Pflex and between groups). PEEP set at two times Pflex did not result in further improvements in oxygenation or oxygen delivery. Tidal volumes were significantly reduced at PEEP above Pflex (Table 2). Increasing PEEP significantly decreased mean arterial pressure in the SW group (92 ± 5 mm Hg after injury to a nadir of 61 ± 8 mm Hg at PEEP at 1.5 times Pflex [p < 0.001]) but did not change in the OA group (Table 1).
Fractional Inflation and Recruitment With PEEP
To compare the dynamic effects of PEEP with the findings during static PV recordings, the respective numbers for PEEP were added to the figures. Fractional recruitment for the different levels of PEEP was at or slightly above the expiratory fractional (de-)recruitment curve (Fig 2, 3). Fractional inflation was significantly above the static deflation limb in the SW group for apex and base, while it was in closer proximity to the deflation limb in the OA group (Fig 2, 3).
Discussion
This study compared OA and SW lung injury models. We found the following: (1) respiratory mechanics and gas exchange were similar in both groups; (2) the amount of edema and poorly aerated tissue were increased in the SW model; (3) hemodynamics showed a more marked increase in pulmonary artery pressure in OA compared to SW; (4) in both models, the inspiratory limb was comparable, but in the expiratory limb a difference between recruitment and inflation was more evident in the SW model; (5) after recruitment, there is no difference between the two models as long as PEEP is > 10 cm H2O, but significantly more collapse occurs at lower levels of PEEP in the basal sections of SW lungs. Our findings suggest that ventilatory setting and in particular the application of PEEP differently affect the lung morphology of the lung in different lung injury models.
Gas Exchange, Hemodynamics, and Lung Volumes
The two models were comparable in terms of gas exchange and respiratory mechanics estimated from the shape of the static PV curve, the magnitude of the Pflex, or the inspiratory pressures, as previously reported by Van der Kloot et al.5 Analysis of total lung, gas, and tissue volumes, however, revealed some unexpected findings: while the decrease in gas volume at expiration was highly comparable for the two models (Table 3), the increase in tissue volume after SW was significantly higher than that observed after OA injury. Consequently, total lung volume at zero end-expiratory pressure did not change in the SW group, while it decreased in the OA group. The increased total tissue volume could theoretically be explained by significant amount of saline solution remaining in the lungs after lavage (217 ± 178 mL in the present study). However, this hypothesis could as well be rejected by the fact that a normal lung would readily absorb saline solution after it has been instilled into the airways. The increase in edema is likely due to the loss/inactivation of surfactant itself causing alterations in the alveolocapillary membrane or due to the large shear stress caused by cyclic reopening and collapse of instable alveoli throughout the ventilatory cycle.272829 The more marked reduction in surfactant and increased edema lead to an increased tendency for partial alveolar collapse in the SW group, as indicated by the increase in poorly aerated lung volume. In addition, the high inspiratory oxygen fraction used in this study may have promoted the occurrence of reabsorption atelectasis due to the alveolar instability especially at low levels of PEEP.3031
Response to PEEP
Increasing PEEP to 0.5 and 1.5 x Pflex significantly improved oxygenation, with the response being more pronounced in the SW group. PEEP set to 2 x Pflex did not result in further improvements in oxygenation or oxygen delivery. The greater response in oxygenation with PEEP was associated with a greater recruitment in the SW group. SW was more likely characterized not only by compression atelectasis due to edema, but also by reabsorption atelectasis and alveolar collapse due to major surfactant depletion, while the opposite may have occurred in the OA group. While cardiac output was maintained in both groups, mean arterial pressure significantly decreased in the SW group. As suggested by the findings of Van der Kloot et al,5 a large increase in lung volume may result in direct compression of the heart in the cardiac fossa, thus impairing left ventricular function.3233 Furthermore, a more pronounced regional heterogeneity of the lung injury induced by SW compared to OA could have played a role.
Whole-Lung and Slice PV Curves, Inflation, and Recruitment
For both models of injury and for two distinct anatomic locations, recruitment parallels inflation throughout the entire inflation limb, but is substantially different from inflation at the deflation limb. The observation that recruitment occurs continuously along the entire inflation limb of the PV curve is in keeping with previous findings171922 and may have important clinical implications: First, the inflation limb of the PV curve may be seen as an equivalent to a recruitment-pressure curve, confirming theoretical analysis.34 Second, setting PEEP according to the inspiratory Pflex seems not to have a good pathophysiologic rationale. At this level of PEEP, only approximately 25% of the recruitment had been accomplished in two models of injury. These data correlated well with previous findings in OA-injured dogs17 and further support the interpretation of the inspiratory Pflex as the pressure threshold of inspiratory recruitment.22 Third, the difference in inflation and recruitment on the deflation limb casts doubt on the usefulness of the expiratory whole-lung PV curve to set PEEP. This approach was based on the well-appreciated findings that PEEP is an expiratory phenomenon and ventilation takes place on the deflation side of the PV envelope.2235 For two models and two anatomic locations studied, the deflation limb of the whole-lung PV curve basically reflected the removal of gas (deflation), but not (de-)recruitment. In addition, fractional recruitment obtained by ventilation with PEEP was at or above the corresponding line of recruitment on the deflation limb and cannot be predicted from the shape of the static whole-lung PV curve. Especially the PMC on the deflation limb, suggested to identify the pressure needed to maintain the lung open at end-expiration,25 showed no correlation to the PMC on the expiratory recruitment curves: In fact, the PMC for the whole-lung PV (26 ± 3 cm H2O for the SW group and 27 ± 4 cm H2O for OA-injured animals) was closely related to the PMC detected on the regional deflation curves. On the contrary, the PMC for the deflation (de-)recruitment curves was significantly lower, ranging from 9 ± 2 cm H2O in the SW group to 13 ± 3 cm H2O in OA-injured animals at the lung base.
When looking at the fractional recruitment maintained at zero end-expiratory pressure after inspiration, there were marked differences between lung apex and lung base: while at lung apex, 60% of recruitment was maintained in SW lungs, only 35% recruitment was left in OA-injured lungs. At lung base, only 25% of recruited volume was left in SW lungs, compared to > 50% in OA-injured lungs. This suggests possible regional heterogeneity in the response to recruitment maneuvers in different models. These differences might be explained, at least in part, by different pathophysiology of injury and by the different regional mechanical relationships between the rib cage and the lung in the apex and in the base, respectively. The SW group was characterized by increased lung edema compared to OA; thus, we would expect more tendency to collapse after recruitment in the most basal regions of the lung, with higher absolute amount of atelectatic tissue and higher lung height from ventral to dorsal regions compared to the apex.36 However, the differences in the amount of fractional recruitment in the base could have affected different distribution of regional pleural pressures in the apex, leading to higher fractional recruitment in the apex in the SW model.3738 This regional heterogeneity of the lung injury could also partially explain different hemodynamic responses to PEEP between the models.
Limitations of the Study
Using CT, we analyzed the morphologic relationships between findings obtained during static PV recording and during subsequent ventilation with PEEP. Unfortunately, scanning of the entire lung during recording of the PV curve is not feasible, and therefore we limited all analyses to two slices: lung apex and lung base. These positions were selected to account for the steep craniocaudal gradient observed in injured lungs and the large lung volume changes at different airway pressures.39 As the degree of displacement was almost identical for comparable pressures during conventional ventilation and PV recording, differences observed during static PV recordings and PEEP cannot be attributed to the problem of displacement. We used CT as a research tool, and we do not want to suggest this method to optimize PEEP selection at the bedside. In fact, just because a region is partially aerated and therefore classified as recruited does not mean that it is no longer subject to an interfacial tension-mediated injury mechanism.
Even more important, the different time scales for the static PV curve and the conventional ventilation limit the comparability of the findings during static PV recording and PEEP-induced changes, as time-dependent reopening of collapsed or flooded lung regions during conventional ventilation may have normalized the static PV curve. That problem, however is inherent to each strategy using a PV relationship to adjust ventilator settings.21 In light of these limitations, our findings suggest the following: (1) PV shape parameters are not useful for lung recruitment and derecruitment estimation in both OA and SW ALI models; and (2) different models can differently affect the influence of different mechanical ventilatory strategies on ventilator-induced lung injury.
Footnotes
Abbreviations: ALI = acute lung injury; HU = Hounsfield unit; OA = oleic acid; PEEP = positive end-expiratory pressure; Pflex = lower inflection point; PMC = point of maximum curvature; PV = pressure volume; SW = saline solution washout
Supported in part by a personal research grant (Dr. Luecke) from the Faculty of Clinical Medicine Mannheim.
The authors have no conflict of interest to disclose.
Received for publication November 30, 2005. Accepted for publication February 9, 2006.
References
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