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Effect of recruitment and body positioning on lung volume and oxygenation in acute lung injury model.

In addition to lung-protective ventilation, the modalities currently being tested in the hope of better oxygenation and lower mortality in patients with acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) include recruitment manoeuvres (RM), prone positioning, various levels of positive end-expiratory pressure (PEEP) and high-frequency oscillatory ventilation (1-5). It has been known for some time that the effect of the interventions mentioned above differ according to factors such as patient position and aetiology of lung injury (2,6,7). However, underlying mechanisms of these interventions are still unclear and require more investigation, especially when these methods are used in combination.

Generation of transpulmonary pressure sufficient to exceed airway opening pressure, elimination of lung compression by the heart, non-gravitational distribution of perfusion and attenuation of lung injury have been proposed as mechanisms for the effect of prone positioning (8-12). RMs are known to recruit collapsed alveoli and convert them into gas-exchanging alveoli, but a relatively high PEEP is required to maintain its effect (13-15).

Considering the fact that pulmonary blood flow is distributed preferentially to the dorsal area regardless of whether the body position is supine or prone (12,16) and that ventilation/perfusion match is critical to oxygenation, it is important to know how effectively aeration is distributed to understand oxygenation improvements after RMs or prone positioning. Prone positioning is associated with a better preservation of the oxygenating effect of RMs compared to the supine position (7,17). It was shown qualitatively that RMs in the supine position (18) or prone positioning (19) improved aeration in dorsal lung areas. However, studies comparing the effect of RMs between supine and prone positions in terms of whole lung volume, especially the effectively aerated lung volumes, are lacking.

In this study, volume analysis of the whole lung with spiral computed tomography (CT) was used to analyse and compare the change in the lung volume between supine and prone positions. In addition, the improvement of oxygenation and the change of lung volume after RMs depending on body position (supine vs. prone) were assessed.

MATERIALS AND METHODS

Animal preparation and measurements Twelve male mongrel dogs (24.7 [+ or -] 2.2 kg, mean [+ or -] SD) were included in this study, using a protocol approved by the committee on the care and use of animals in research of Seoul National University Hospital. Each dog was anaesthetised with an intramuscular injection of ketamine hydrochloride 2 mg/kg (Ketalar, Yuhan Yanghang, Seoul, Korea), xylazine hydrochloride 1 mg/kg (Rompun, Bayer Korea, Seoul, Korea) and continuous infusions of vecuronium bromide (0.2 mg/kg/h) and xylazine hydrochloride (0.02 mg/kg/h). All dogs received intravenous 0.9% saline at a rate of 100 ml/h throughout the experiment.

Volume-controlled mechanical ventilation was initiated using a Servo 900C ventilator (Siemens, Erlangen, Germany) with a tidal volume of 10 ml/kg, a frequency of 12 breaths/minutes, zero PEEP and an Fi[O.sub.2] of 0.8. Systemic arterial pressure, pulmonary artery pressure, central venous pressure and cardiac output were measured. Whole lung spiral CT scans (MX 8000; Philips Inc, Best, Netherlands) were also obtained.

Experimental protocol

Three equally divided doses of oleic acid (0.09 ml/kg) (Sigma, Steinheim, Germany) were slowly injected through the proximal port of the pulmonary artery catheter in supine, left and right lateral positions at five-minute intervals (20). After a 90-minute stabilisation period in the supine position, the decrease of [P.sub.a][O.sub.2]/Fi[O.sub.2] ratio below 200 was used to confirm ALI.

[FIGURE 1 OMITTED]

Haemodynamic and respiratory variables, arterial blood gas analysis and CT scans were obtained before (baseline) and 90 minutes after oleic acid administration (OA 90) and also five minutes before and after each RM. At the time of position change (90 minutes after oleic acid administration), PEEP was increased to 3 cm[H.sub.2]O. RMs were composed of four consecutive 15 second inflations at 35 cm[H.sub.2]O of airway pressure with two- to three-second intervals at 3 cm[H.sub.2]O in between. A schematic diagram of the experimental protocol is shown in Figure 1.

Acquisition and analysis of data

Haemodynamic and ventilatory variables were obtained directly from the monitor and the ventilator. CT scans were performed at functional residual capacity. The whole lung underwent volume analysis after dividing each section of the lung into dorsal and ventral parts using the pulmonary trunk as the reference level. Each divided lung section was categorised according to their Hounsfield unit (HU) into hyperinflated (-1000~-900 HU), well-aerated (-900~-500 HU), poorly-aerated (-500~-100 HU) and non-aerated (-100~100 HU) volumes and analysed with Rapidia[R] 2.7 (3DMED, Seoul, Korea), a volume- and Hounsfield unit-calculating software.

Statistical analysis

All data are expressed as mean [+ or -] SD. SPSS 12.0 for windows (SPSS Inc, Chicago, IL, USA) was used for statistical analyses. Wilcoxon signed rank test was used to compare variables between baseline and OA 90. Using repeated measures analysis of variance, stages RM I-5, RM II-5 and RM III-5 were analysed to detect changes according to the time after positioning. One sample t-test was used to compare stages before and after the RM, and to evaluate the effects of positioning. Pearson's correlation coefficient was used to search for variables that correlate with [P.sub.a][O.sub.2] changes.

RESULTS

There was no difference in haemodynamic and respiratory variables between the two groups at baseline and OA 90. In the supine group, there were no differences between stages OA 90, RM I-5, RM II-5 and RM III-5 in [P.sub.a][O.sub.2], [P.sub.a]C[O.sub.2] and lung volumes whereas in the prone group, there was a difference in [P.sub.a][O.sub.2], [P.sub.a]C[O.sub.2] and lung volumes among stages RM I-5, RM II-5 and RM III-5. Haemodynamic variables remained stable throughout the experiment in both groups. Respiratory variables of both groups are shown in Table 1.

[FIGURE 2 OMITTED]

Effect of recruitment manoeuvres

In the supine group, recruitment manoeuvres increased [P.sub.a][O.sub.2] from 83 [+ or -] 32 mmHg (mean [+ or -] SD) to 114 [+ or -] 64 mmHg (P=0.025) but the effects were not sustained (Table 1). Variables that correlated with the increase of [P.sub.a][O.sub.2] include the decrease of peak (P=0.042) and plateau (P=0.001) airway pressure, and the increase of poorly- and well-aerated dependent (dorsal) lung volume (P = 0.016) (Figure 2).

[FIGURE 3 OMITTED]

In the prone group, RMs failed to improve oxygenation. However, peak (P=0.005) and plateau (P=0.018) airway pressures decreased and poorly- and well-aerated dependent (ventral) lung volume (P=0.002) increased after RMs (Figure 2).

Effect of body positioning

The effect of body positioning was determined by comparing variables of OA 90 with those obtained five minutes before each RM. In the prone group, there was an increase in [P.sub.a][O.sub.2] (P=0.004), which correlated with the increase in poorly- and well-aerated dorsal (nondependent) lung volume (r=0.787, P <0.001) (Figure 3). Stages following RM II-5 showed a continuous elevation of [P.sub.a][O.sub.2] (P <0.05) (Table 1). There were no changes in [P.sub.a][O.sub.2] in the supine group.

DISCUSSION

Our study's main findings are 1) RMs produced an increase in [P.sub.a][O.sub.2] in the supine position, which correlated with the increase in the poorly- and well-aerated dorsal (dependent) lung volume, but did not produce an increase in [P.sub.a][O.sub.2] in the prone position despite an increase of poorly- and well-aerated ventral (dependent) lung volume and 2) prone positioning by itself produced an increase in [P.sub.a][O.sub.2], which correlated with the increase in the poorly- and well-aerated dorsal (nondependent) lung volume.

In our study, RMs in the supine group produced an increase in [P.sub.a][O.sub.2], which correlated with the increase of poorly- and well-aerated dorsal (dependent) lung volume. Peak and plateau pressures were also decreased after each RM. However, neither effect was sustained. In accord with most studies concerning ARDS or ALI, the majority of alveolar collapse and consolidation was observed in the dorsal (dependent) lung (17,18). Therefore, alveolar recruitment of the dorsal lung and subsequent improvement of ventilation/perfusion match seems to be the cause of improved oxygenation because perfusion is preferentially distributed to the dorsal lung irrespective of body position (16,21).

Previous studies concerning the effect of RMs in the supine position have shown that an 'anti-derecruitment strategy', such as high PEEP, is important in maintaining the effect of RM (7,22,23). In our study, the effect of RMs in terms of oxygenation seemed to disappear within one hour as indicated by [P.sub.a][O.sub.2] measured 55 minutes after RMs and the relatively low PEEP is thought to be the cause of the derecruitment following the RMs.

In the prone group, although the RMs increased the poorly- and well-aerated dependent (ventral) lung volume, it failed to increase the [P.sub.a][O.sub.2]. There may be a few explanations for the failure to improve oxygenation after RMs despite increase of the poorly- and well-aerated dependent (ventral) lung volume. As demonstrated by a recent study from the ARDSnet regarding the effect of RMs with high PEEP in the supine position (15), recruitable lung volume is one of the important factors that determine the effectiveness of RMs. However, in the prone position, most of the recruitable lung volume in the dorsal lung is already recruited by the prone positioning and pulmonary blood flow is preferentially distributed to the dorsal lung (10,12,16,21). Therefore, the recruitment of ventral (dependent) lung volume and improved respiratory compliances reflected in peak and plateau pressures had little effect on the improvement of ventilation/perfusion mismatch.

In contrast to the supine group, prone positioning was associated with a significant increase in [P.sub.a][O.sub.2] that correlated with the increase of poorly- and well-aerated dorsal (nondependent) lung volume. The improved oxygenation was sustained irrespective of RMs. Another finding worth noting is that the [P.sub.a]C[O.sub.2] decreased after 90 minutes of prone positioning and remained so. This was not observed in the supine group, implying that prone positioning not only improved oxygenation but also alveolar ventilation as well.

The proposed mechanisms of RMs and prone positioning seem different, but these two widely used and studied methods share a fundamental aspect, alveolar recruitment. RMs recruit alveoli by applying supernormal airway pressure (23,24) and prone positioning recruits alveoli by producing favourable pressure gradients (2,25) both resulting in improved oxygenation. However, in order to maintain the oxygenation-improving effect after RMs, anti-derecruitment measures are needed. Proposed anti-derecruitment strategies include high PEEP, prone positioning and small tidal volume ventilation with optimal PEEP (7,23,24,26).

The results of our study suggest that recruitment of the dorsal lung volume is a shared mechanism of oxygenation improvement after RM and prone positioning. As stated above, maintenance of the dorsal lung perfusion regardless of body position seems to play a pivotal role (10,12,16).

Although there may be contradictory views, we agree with the viewpoint that CT analysis using the whole lung is more reliable compared to analysis of a few representative sections, especially when studying ALI or ARDS. CT scanning and analysis of the whole lung provides a better understanding of changes in lung volume and density. Unfortunately, the information derived from lung CT scans is limited to lung aeration. Lung perfusion is a major factor in determining oxygenation, which cannot be detected by lung CT scans. Since the ventilation/perfusion match is a critical factor in determining oxygenation, CT scans alone are not sufficient to assess a definite gas exchange-lung structure relationship.

There are some limitations in this study that need to be considered when interpreting the results. In the prone group, there may be a possibility that the preceding RM may have influenced the effect of the following RM, since the prone position is known to attenuate derecruitment after RM (7). When before-RM stages were analysed by using repeated measures ANOVA, there was a significant difference in [P.sub.a][O.sub.2], respiratory mechanics and lung volumes in the prone group. Because there were no changes in [P.sub.a][O.sub.2] after RM and the applied PEEP level was only 3 cm[H.sub.2]O, the possibility that the preceding RM may have affected the following RM one hour later seems to be low. The increase in oxygenation is most likely the result of prone positioning itself rather than RMs in the prone group.

In the supine group, repeated ANOVA measures showed no difference among three stages before RM, implying that conditions before each RM were comparable. Considering the level of applied PEEP (3 cm[H.sub.2]O) and the negative results of other studies that applied higher levels of PEEP (10 to 14 cm[H.sub.2]O) (7,10,14), the one-hour interval between RMs seems to be sufficient to exclude the effect of the previous RM.

As mentioned above, the level of PEEP used in this study is very low compared to other studies and to PEEPs used clinically. The focus of this study was to highlight the mechanism of improved oxygenation of RMs and prone positioning and the level of PEEP was intentionally chosen to serve this purpose.

In conclusion, our study suggests that increased [P.sub.a][O.sub.2] after RM in the supine position or after prone positioning is related to the increase of poorly- and well-aerated dorsal lung volume in the ALI model.

RMs were shown to preferentially recruit dependent lung areas regardless of body position.

REFERENCES

(1.) Mancebo J, Fernandez R, Blanch L, Rialp G, Gordo F, Ferrer M. A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome. Am J Respir Crit Care Med 2006; 173:1233-1239.

(2.) Demory D, Michelet P, Arnal JM, Donate S, Forel JM, Gainnier M. High frequency oscillatory ventilation following prone positioning prevents a further impairment in oxygenation. Crit Care Med 2007; 35:106-111.

(3.) Mercat A, Richard JC, Vielle B, Jaber S, Osman D, Diehl JL. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299:646-655.

(4.) Meade MO, Cook DJ, Guyatt GH, Slutsky AS, Arabi YM, Cooper DJ. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299:637-645.

(5.) Gattinoni L, Caironi P, Cressoni M, Chiumello D, Ranieri VM. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 2006; 354:1775-1786.

(6.) Papazian L, Gainnier M, Marin V, Donati S, Arnal JM, Demory D. Comparison of prone positioning and high-frequency oscillatory ventilation in patients with acute respiratory distress syndrome. Crit Care Med 2005; 33:2162-2171.

(7.) Lim CM, Jung H, Koh Y, Lee JS, Shim TS, Lee SD. Effect of alveolar recruitment maneuver in early acute respiratory distress syndrome according to antiderecruitment strategy, etiological category of diffuse lung injury, and body position of the patient. Crit Care Med 2003; 31:411-418.

(8.) Albert RK, Hubmayr RD. The prone position eliminates compression of the lungs by the heart. Am J Respir Crit Care Med 2000; 161:1660-1665.

(9.) Ball WS, Wicks JD, Mettler FA Jr. Prone-supine change in organ position: CT demonstration. AJR Am J Roentgenol 1980; 135:815-920.

(10.) Wiener CM, Kirk W, Albert RK. Prone position reverses gravitational distribution of perfusion in dog lungs with oleic acid-induced injury. J Appl Physiol 1990; 68:1386-1392.

(11.) Broccard A, Shapiro RS, Schmitz LL, Adams AB, Nahum A, Marini JJ. Prone positioning attenuates and redistributes ventilator-induced lung injury in dogs. Crit Care Med 2000; 28:295-303.

(12.) Glenny RW, Lamm WJ, Albert RK, Robertson HT. Gravity is a minor determinant of pulmonary blood flow distribution. J Appl Physiol 1991; 71:620-629.

(13.) Grasso S, Mascia L, Del Turco M, Malacarne P, Giunta F, Brochard L. Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002; 96:795-802.

(14.) Villagra A, Ochagavia A, Vatua S, Murias G, Fernandez MD, Aguilar JL. Recruitment maneuvers during lung protective ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med 2002; 165:165-170.

(15.) The ARDS trials network. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratory distress syndrome ventilated with high positive end-expiratory pressure. Crit Care Med 2003; 31:2592-2610.

(16.) Nyren S, Mure M, Jacobsson H, Larsson SA, Lindahl S. Pulmonary perfusion is more uniform in the prone than in the supine position: scintigraphy in healthy humans. J Appl Physiol 1999; 86:1135-1141.

(17.) 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; 161:1949-1956.

(18.) Gattinoni L, Pesenti A, Bombino M, Baglioni S, Rivolta M, Rossi F. Relationship between lung computed tomographic density, gas exchange, and PEEP in acute respiratory failure. Anesthesiology 1988; 69:824-832.

(19.) Papazian L, Paladini MH, Bregeon F, Thirion X, Durieux O, Gainnier M. Can the tomographic aspect characteristics of patients presenting with acute respiratory distress syndrome predict improvement in oxygenation related response to the prone position? Anesthesiology 2002; 97:599-607.

(20.) Pelosi P, Goldner M, McKibben A, Adams A, Eccher G, Caironi P. Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med 2001; 164:122-130.

(21.) Schuster DP, Haller J. Effects of body position on regional pulmonary blood flow during acute pulmonary edema in dogs: A positron emission tomography study. J Crit Care 1991; 6:19-28.

(22.) Pelosi P, Cadringher P, Bottino N, Panigada M, Carrieri F, Riva E. Sigh in acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 159:872-880.

(23.) 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; 26:501-507.

(24.) Patroniti N, Foti G, Cortinovis B, Maggioni E, Bigatello LM, Cereda M. Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation. Anesthesiology 2002; 96:788-794.

(25.) Albert RK, Leasa D, Sanderson M, Robertson HT, Hlastala MP. The prone position improves arterial oxygenation and reduces shunt in oleic-acid-induced acute lung injury. Am Rev Respir Dis 1987; 135:628-633.

(26.) Rimensberger PC, Pristine G, Mullen JBM, Cox PN, Slutsky AS. Lung recruitment during small tidal volume ventilation allows minimal positive end-expiratory pressure without augmenting lung injury. Crit Care Med 1999; 27:1940-1945.

H. G. RYU *, J.-H. BAHK [[dagger]], H.-J. LEE [[double dagger]], J.-G. IM [[section]]

Departments of Anesthesiology and Radiology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea

* M.D., Ph.D., Instructor, Department of Anesthesiology.

[[dagger]] M.D., Ph.D., Associate Professor, Department of Anesthesiology.

[[double dagger]] M.D., Ph.D., Assistant Professor, Department of Radiology.

[[section]] M.D., Ph.D., Professor, Department of Radiology.

Address for reprints: Dr J.-H. Bahk, Department of Anesthesiology, Seoul National University Hospital, 28 Yongon-dong, Jongno-gu, Seoul 110-744, Korea.

Accepted for publication on July 7, 2008.
TABLE 1
Respiratory variables

Variable Baseline

Supine group
 [P.sub.a][O.sub.2] (mmHg) 333 [+ or -] 50
 [P.sub.a]C[O.sub.2] (mmHg) 48.2 [+ or -] 4.8
 Peak pressure (cm[H.sub.2]O) 9.2 [+ or -] 0.8
 Plateau pressure (cm[H.sub.2]O) 7.6 [+ or -] 0.6

Prone group
 [P.sub.a][O.sub.2] (mmHg) 329 [+ or -] 46
 [P.sub.a]C[O.sub.2] (mmHg) 45.6 [+ or -] 3.8
 Peak pressure (cm[H.sub.2]O) 9.7 [+ or -] 0.7
 Plateau pressure (cm[H.sub.2]O) 8.3 [+ or -] 0.7

Variable OA 90

Supine group
 [P.sub.a][O.sub.2] (mmHg) 75 [+ or -] 32
 [P.sub.a]C[O.sub.2] (mmHg) 67.2 [+ or -] 11.7
 Peak pressure (cm[H.sub.2]O) 13.6 [+ or -] 2.4
 Plateau pressure (cm[H.sub.2]O) 11.7 [+ or -] 2.3

Prone group
 [P.sub.a][O.sub.2] (mmHg) 77 [+ or -] 31
 [P.sub.a]C[O.sub.2] (mmHg) 66.2 [+ or -] 20.7
 Peak pressure (cm[H.sub.2]O) 16.6 [+ or -] 1.7
 Plateau pressure (cm[H.sub.2]O) 14.7 [+ or -] 1.2

Variable RM I-5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 77 [+ or -] 30
 [P.sub.a]C[O.sub.2] (mmHg) 68.5 [+ or -] 8.2
 Peak pressure (cm[H.sub.2]O) 17.7 [+ or -] 1.5
 Plateau pressure (cm[H.sub.2]O) 15.5 [+ or -] 1.8

Prone group
 [P.sub.a][O.sub.2] (mmHg) 152 [+ or -] 98
 [P.sub.a]C[O.sub.2] (mmHg) 67.6 [+ or -] 22.7
 Peak pressure (cm[H.sub.2]O) 19.6 [+ or -] 1.9
 Plateau pressure (cm[H.sub.2]O) 17.8 [+ or -] 1.8

Variable RM I+5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 102 [+ or -] 42 *
 [P.sub.a]C[O.sub.2] (mmHg) 70.4 [+ or -] 12.2
 Peak pressure (cm[H.sub.2]O) 15.3 [+ or -] 2.4 *
 Plateau pressure (cm[H.sub.2]O) 13 [+ or -] 2.8 *

Prone group
 [P.sub.a][O.sub.2] (mmHg) 151 [+ or -] 104
 [P.sub.a]C[O.sub.2] (mmHg) 64.2 [+ or -] 18.8
 Peak pressure (cm[H.sub.2]O) 18.1 [+ or -] 2.2 *
 Plateau pressure (cm[H.sub.2]O) 15.6 [+ or -] 1.8 *

Variable RM II-5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 91 [+ or -] 40
 [P.sub.a]C[O.sub.2] (mmHg) 65.2 [+ or -] 10.3
 Peak pressure (cm[H.sub.2]O) 17.3 [+ or -] 1.7
 Plateau pressure (cm[H.sub.2]O) 15.3 [+ or -] 2.3

Prone group
 [P.sub.a][O.sub.2] (mmHg) 198 [+ or -] 109 ([dagger])
 [P.sub.a]C[O.sub.2] (mmHg) 55.4 [+ or -] 14.2 ([dagger])
 Peak pressure (cm[H.sub.2]O) 20.2 [+ or -] 1.8
 Plateau pressure (cm[H.sub.2]O) 18.1 [+ or -] 1.6

Variable RM II+5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 108 [+ or -] 66 *
 [P.sub.a]C[O.sub.2] (mmHg) 65.6 [+ or -] 11.5
 Peak pressure (cm[H.sub.2]O) 16.3 [+ or -] 2.1 *
 Plateau pressure (cm[H.sub.2]O) 13.7 [+ or -] 2.6 *

Prone group
 [P.sub.a][O.sub.2] (mmHg) 216 [+ or -] 118 ([dagger])
 [P.sub.a]C[O.sub.2] (mmHg) 53.6 [+ or -] 12.5 ([dagger])
 Peak pressure (cm[H.sub.2]O) 18.8 [+ or -] 2.5 *
 Plateau pressure (cm[H.sub.2]O) 16.4 [+ or -] 2.3 *

Variable RM III-5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 82 [+ or -] 35
 [P.sub.a]C[O.sub.2] (mmHg) 58.0 [+ or -] 24.3
 Peak pressure (cm[H.sub.2]O) 19.2 [+ or -] 2.3
 Plateau pressure (cm[H.sub.2]O) 16.1 [+ or -] 2.8

Prone group
 [P.sub.a][O.sub.2] (mmHg) 259 [+ or -] 90 ([dagger])
 [P.sub.a]C[O.sub.2] (mmHg) 47.2 [+ or -] 7.9 ([dagger])
 Peak pressure (cm[H.sub.2]O) 21 [+ or -] 1.8
 Plateau pressure (cm[H.sub.2]O) 18.8 [+ or -] 1.4

Variable RM III+5

Supine group
 [P.sub.a][O.sub.2] (mmHg) 133 [+ or -] 93 *
 [P.sub.a]C[O.sub.2] (mmHg) 55.5 [+ or -] 20.2
 Peak pressure (cm[H.sub.2]O) 17.5 [+ or -] 2.1 *
 Plateau pressure (cm[H.sub.2]O) 15.2 [+ or -] 2.7 *

Prone group
 [P.sub.a][O.sub.2] (mmHg) 256 [+ or -] 83 ([dagger])
 [P.sub.a]C[O.sub.2] (mmHg) 48.4 [+ or -] 7.5 ([dagger])
 Peak pressure (cm[H.sub.2]O) 19.8 [+ or -] 3.0 *
 Plateau pressure (cm[H.sub.2]O) 17.1 [+ or -] 2.5 *

Data are mean [+ or -] SD. RM = recruitment manoeuvre. * indicates
a P value less than 0.05 compared to values five minutes before RM
when all three RMs are analysed together. ([dagger]) indicates a P
value less than 0.05 compared to OA 90 values. OA 90 = 90 minutes
after oleic acid injection, RM I-5 = five minutes before the first
RM, RM I+5 = five minutes after the first RM, RM II-5 = five
minutes before the second RM, RM II+5 = five minutes after the
second RM, RM III-5 = five minutes before the third RM, RM III+5 =
five minutes after the third RM.
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Author:Ryu, H.G.; Bahk, J.-H.; Lee, H.-J.; Im, J.-G.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:9SOUT
Date:Nov 1, 2008
Words:4204
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