Skip to content

Advertisement

  • Review
  • Open Access

New and conventional strategies for lung recruitment in acute respiratory distress syndrome

  • 1Email author,
  • 2 and
  • 3
Critical Care201014:210

https://doi.org/10.1186/cc8851

  • Published:

Abstract

This article is one of ten reviews selected from the Yearbook of Intensive Care and Emergency Medicine 2010 (Springer Verlag) and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum.com/series/yearbook. Further information about the Yearbook of Intensive Care and Emergency Medicine is available from http://www.springer.com/series/2855.

Keywords

  • Acute Lung Injury
  • Recruitment Maneuver
  • Transpulmonary Pressure
  • Maximum Inspiratory Pressure
  • Lung Recruitment

Introduction

Mechanical ventilation is a supportive and life saving therapy in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Despite advances in critical care, mortality remains high [1]. During the last decade, the fact that mechanical ventilation can produce morphologic and physiologic alterations in the lungs has been recognized [2]. In this context, the use of low tidal volumes (VT) and limited inspiratory plateau pressure (Pplat) has been proposed when mechanically ventilating the lungs of patients with ALI/ARDS, to prevent lung as well as distal organ injury [3]. However, the reduction in VT may result in alveolar derecruitment, cyclic opening and closing of atelectatic alveoli and distal small airways leading to ventilator-induced lung injury (VILI) if inadequate low positive end-expiratory pressure (PEEP) is applied [4]. On the other hand, high PEEP levels may be associated with excessive lung parenchyma stress and strain [5] and negative hemodynamic effects, resulting in systemic organ injury [6]. Therefore, lung recruitment maneuvers have been proposed and used to open up collapsed lung, while PEEP counteracts alveolar derecruitment due to low VT ventilation [4]. Lung recruitment and stabilization through use of PEEP are illustrated in Figure 1. Nevertheless, the beneficial effects of recruitment maneuvers in ALI/ARDS have been questioned. Although Hodgson et al. [7] showed no evidence that recruitment maneuvers reduce mortality or the duration of mechanical ventilation in patients with ALI/ARDS, such maneuvers may be useful to reverse life-threatening hypoxemia [8] and to avoid derecruitment resulting from disconnection and/or airway suctioning procedures [9].
Figure 1
Figure 1

Computed tomography images of oleic acid-induced acute lung injury in dogs at different inspiratory and expiratory pressures. Note the improvement in alveolar aeration at end-expiration after the recruitment maneuver. Large arrows represent inspiration and expiration. Double-ended arrows represent the tidal breathing (end-expiration and end-inspiration). Adapted from [4].

The success and/or failure of recruitment maneuvers are associated with various factors: 1) Different types of lung injury, mainly pulmonary and extra-pulmonary origin; 2) differences in the severity of lung injury; 3) the transpulmonary pressures reached during recruitment maneuvers; 4) the type of recruitment maneuver applied; 5) the PEEP levels used to stabilize the lungs after the recruitment maneuver; 6) differences in patient positioning (most notably supine vs prone); 7) use of different vasoactive drugs, which may affect cardiac output and the distribution of pulmonary blood flow, thus modifying gas-exchange.

Although numerous reviews have addressed the use of recruitment maneuvers to optimize ventilator settings in ALI/ARDS, this issue remains controversial. While some types of recruitment maneuver have been abandoned in clinical practice, new, potentially interesting strategies able to recruit the lungs have not been properly considered. In the present chapter we will describe and discuss: a) Definition and factors affecting recruitment; b) types of recruitment maneuvers; and c) the role of variable ventilation as a recruitment maneuver.

Definition and factors affecting recruitment maneuvers

Recruitment maneuver denotes the dynamic process of an intentional transient increase in transpulmonary pressure aimed at opening unstable airless alveoli, which has also been termed alveolar recruitment maneuver. Although the existence of alveolar closure and opening in ALI/ARDS has been questioned [10], the rationale for recruitment maneuvers is to open the atelectatic alveoli, thus increasing endexpiratory lung volume, improving gas exchange, and attenuating VILI [11]. However, recruitment maneuvers may also contribute to VILI [11, 12], with translocation of pulmonary bacteria [13] and cytokines into the systemic circulation [14]. Furthermore, since recruitment maneuvers increase mean thoracic pressure, they may lead to a reduction in venous return with impairment of cardiac output [15].

Various factors may influence the response to a recruitment maneuver, namely: 1) The nature and extent of lung injury, and 2) patient positioning.

Nature and extent of lung injury

The nature of the underlying injury can affect the response to a recruitment maneuver. In direct (pulmonary) lung injury, the primary structure damaged is the alveolar epithelium resulting in alveolar filling by edema, fibrin, and neutrophilic aggregates. In indirect (extra-pulmonary) lung injury, inflammatory mediators are released from extrapulmonary foci into the systemic circulation leading to microvessel congestion and interstitial edema with relative sparing of intra-alveolar spaces [16]. Therefore, recruitment maneuvers should be more effective to open atelectatic lung regions in indirect compared to direct lung injury. Based on this hypothesis, Kloot et al. [17] investigated the effects of recruitment maneuvers on gas exchange and lung volumes in three experimental models of ALI: Saline lavage or surfactant depletion, oleic acid, and pneumonia, and observed improvement in oxygenation only in ALI induced by surfactant depletion. Riva et al. [18] compared the effects of a recruitment maneuver in models of pulmonary and extrapulmonary ALI, induced by intratracheal and intraperitoneal instillation of Escherichia coli lipopolysaccharide, with similar transpulmonary pressures. They found that the recruitment maneuver was more effective for opening collapsed alveoli in extrapulmonary compared to pulmonary ALI, improving lung mechanics and oxygenation with limited damage to alveolar epithelium. Using electrical impedance and computed tomography (CT) to assess lung ventilation and aeration, respectively, Wrigge et al. [19] suggested that the distribution of regional ventilation was more heterogeneous in extrapulmonary than in pulmonary ALI during lung recruitment with slow inspiratory flow. However, this phenomenon and the claim that recruitment maneuvers are useful to protect the so called 'baby lung', i.e., the lung tissue that is usually present in ventral areas and receives most of the tidal ventilation, has been recently challenged. According to Grasso et al. [20], recruitment maneuvers combined with high PEEP levels can lead to hyperinflation of the baby lung due to inhomogeneities in the lung parenchyma, independent of the origin of the injury (pulmonary or extrapulmonary).

Recently, we assessed the impact of recruitment maneuvers on lung mechanics, histology, inflammation and fibrogenesis at two different degrees of lung injury (moderate and severe) in a paraquat ALI model [21]. While both degrees of injury showed comparable amounts of lung collapse, severe ALI was accompanied by alveolar edema. After a recruitment maneuver, lung mechanics improved and the amount of atelectasis was reduced to similar extents in both groups, but in the presence of alveolar edema, the recruitment maneuver led to hyperinflation, and triggered an inflammatory as well as a fibrogenic response in the lung tissue.

Patient positioning

Prone positioning may not only contribute to the success of recruitment maneuvers, but should itself be considered as a recruitment maneuver. In the prone position, the transpulmonary pressure in dorsal lung areas increases, opening alveoli and improving gas-exchange [22]. Some authors have reported that in healthy [23], as well as in lung-injured animals [24], mechanical ventilation leading to lung overdistension and cyclic collapse/reopening was associated with less extensive histological change in dorsal regions in the prone, as compared to the supine position. Although the claim that body position affects the distribution of lung injury has been challenged, the development of VILI due to excessively high VT seems to be delayed during prone compared to supine positioning [25].

The reduction or delay in the development of VILI in the prone position can be explained by different mechanisms: (a) A more homogeneous distribution of transpulmonary pressure gradient due to changes in the lung-thorax interactions and direct transmission of the weight of the abdominal contents and heart [22], yielding a redistribution of ventilation; (b) increased end-expiratory lung volume resulting in a reduction in stress and strain [25]; and (c) changes in regional perfusion and/or blood volume [26]. In a paraquat model of ALI, the prone position was associated with a better perfusion in ventral and dorsal regions, a more homogeneous distribution of alveolar aeration which reduced lung mechanical changes and increased end expiratory lung volume and oxygenation [27]. In addition, the prone position reduced alveolar stress but no regional changes were observed in inflammatory markers. Recruitment maneuvers also improved oxygenation more effectively with a decreased PEEP requirement for preservation of the oxygenation response in prone compared with supine position in oleic acid-induced lung injury [28]. Those findings suggest that the prone position may protect the lungs against VILI, and recruitment maneuvers can be more effective in the prone compared to the supine position.

Types of recruitment maneuver

A wide variety of recruitment maneuvers has been described. The most relevant are represented by: Sustained inflation maneuvers, high pressure controlled ventilation, incremental PEEP, and intermittent sighs. However, the best recruitment maneuver technique is currently unknown and may vary according to the specific circumstances.

The most commonly used recruitment maneuver is the sustained inflation technique, in which a continuous pressure of 40 cmH2O is applied to the airways for up to 60 sec [8]. Sustained inflation has been shown to be effective in reducing lung atelectasis [29], improving oxygenation and respiratory mechanics [18, 29], and preventing endotracheal suctioning-induced alveolar derecruitment [9]. However, the efficacy of sustained inflation has been questioned and other studies showed that this intervention may be ineffective [30], short-lived [31], or associated with circulatory impairment [32], an increased risk of baro/volutrauma [33], a reduced net alveolar fluid clearance [34], or even worsened oxygenation [35].

In order to avoid such side effects, other types of recruitment maneuver have been developed and evaluated. The most important are: 1) incrementally increased PEEP limiting the maximum inspiratory pressure [36]; 2) pressure-controlled ventilation applied with escalating PEEP and constant driving pressure [30]; 3) prolonged lower pressure recruitment maneuver with PEEP elevation up to 15 cmH2O and end inspiratory pauses for 7 sec twice per minute during 15 min [37]; 4) intermittent sighs to reach a specific plateau pressure in volume or pressure control mode [38]; and 5) long slow increase in inspiratory pressure up to 40 cmH2O (RAMP) [18].

Impact of recruitment maneuver on ventilator-induced lung injury

While much is known about the impact of recruitment maneuvers on lung mechanics and gas exchange, only a few studies have addressed their effects on VILI. Recently, Steimback et al. [38] evaluated the effects of frequency and inspiratory plateau pressure (Pplat) during recruitment maneuvers on lung and distal organs in rats with ALI induced by paraquat. They observed that although a recruitment maneuver with standard sigh (180 sighs/hour and Pplat = 40 cmH2O) improved oxygenation and decreased PaCO2, lung elastance, and alveolar collapse, it resulted in hyperinflation, ultrastructural changes in alveolar capillary membrane, increased lung and kidney epithelial cell apoptosis, and type III procollagen (PCIII) mRNA expression in lung tissue. On the other hand, reduction in the sigh frequency to 10 sighs/hour at the same Pplat (40 cmH2O) diminished lung elastance and improved oxygenation, with a marked decrease in alveolar hyperinflation, PCIII mRNA expression in lung tissue, and apoptosis in lung and kidney epithelial cells. However, the association of this sigh frequency with a lower Pplat of 20 cmH2O worsened lung elastance, histology and oxygenation, and increased PaCO2 with no modifications in PCIII mRNA expression in lung tissue and epithelial cells apoptosis of distal organs. Figure 2 illustrates some of these effects. We speculate that there is a sigh frequency threshold beyond which the intrinsic reparative properties of the lung epithelium are over-whelmed. Although the optimal sigh frequency may be different in healthy animals/patients compared to those with ALI, our results suggest that recruitment maneuvers with high frequency or low plateau pressure should be avoided. Theoretically, a recruitment maneuver using gradual inflation of the lungs may yield a more homogeneous distribution of pressure throughout the lung parenchyma, avoiding repeated maneuvers and reducing lung stretch while allowing effective gas exchange.
Figure 2
Figure 2

Percentage of change in static lung elastance (Est, L), oxygenation (PaO 2 ), fractional area of alveolar collapse (Coll) and hyperinflation (Hyp), and mRNA expression of type III procollagen (PCIII) from sustained inflation (SI) and sigh at different frequencies (10, 15 and 180 per hour) to non-recruited acute lung injury rats. Note that at low sigh frequency, oxygenation and lung elastance improved, followed by a reduction in alveolar collapse and PCIII. Adapted from [38].

Riva et al. [18] compared the effects of sustained inflation using a rapid high recruitment pressure of 40 cmH2O for 40 sec with a progressive increase in airway pressure up to 40 cmH2O reached at 40 sec after the onset of inflation (so called RAMP) in paraquat-induced ALI. They reported that the RAMP maneuver improved lung mechanics with less alveolar stress. Among other recruitment maneuvers proposed as alternatives to sustained inflation, RAMP may differ according to the time of application and the mean airway pressure.

Recently, Saddy and colleagues [39] reported that assisted ventilation modes such as assist-pressure controlled ventilation (APCV) and biphasic positive airway pressure associated with pressure support Ventilation (BiVent+PSV) led to alveolar recruitment improving gas-exchange and reducing inflammatory and fibrogenic mediators in lung tissue compared to pressure controlled Ventilation. They also showed that BiVent+PSV was associated with less inspiratory effort, reduced alveolar capillary membrane injury, and fewer inflammatory and fibrogenic mediators compared to APCV [39].

The role of variable ventilation as a recruitment maneuver

Variable mechanical ventilation patterns are characterized by breath-by-breath changes in VT that mimic spontaneous breathing in normal subjects, and are usually accompanied by reciprocal changes in the respiratory rate. Time series of VT and respiratory rate values during variable mechanical ventilation may show long-range correlations, which are more strictly 'biological', or simply random (noisy). Both biological and noisy patterns of variable mechanical ventilation have been shown to improve oxygenation and respiratory mechanics, and reduce diffuse alveolar damage in experimental ALI/ARDS [40, 41]. Although different mechanisms have been postulated to explain such findings, lung recruitment seems to play a pivotal role.

Suki et al. [42] showed that once the critical opening pressure of collapsed airways/alveoli was exceeded, all subtended or daughter airways/alveoli with lower critical opening pressure would be opened in an avalanche. Since the critical opening pressure values of closed airways as well as the time to achieve those values may differ through the lungs, mechanical ventilation patterns that produce different airway pressures and inspiratory times may be advantageous to maximize lung recruitment and stabilization, as compared to regular patterns. Accordingly, variable controlled mechanical ventilation has been reported to improve lung function in experimental models of atelectasis [43] and during one-lung ventilation [44]. In addition, Boker et al. [45] reported improved arterial oxygenation and compliance of the respiratory system in patients ventilated with variable compared to conventional mechanical ventilation during surgery for repair of abdominal aortic aneurysms, where atelectasis is likely to occur due to increased intra-abdominal pressure.

There is increasing experimental evidence suggesting that variable mechanical ventilation represents a more effective way of recruiting the lungs than conventional recruitment maneuvers. Bellardine et al. [46] showed that recruitment following high VT ventilation lasted longer with variable than with monotonic ventilation in excised calf lungs. In addition, Thammanomai et al. [47] showed that variable ventilation improved recruitment in normal and injured lungs in mice. In an experimental lavage model of ALI/ARDS, we recently showed that oxygenation improvement following a recruitment maneuver through sustained inflation was more pronounced when combined with variable mechanical ventilation [41]. Additionally, the redistribution of pulmonary blood flow from cranial to caudal and from ventral to dorsal lung zones was higher and diffuse alveolar damage less when variable ventilation was associated with the ventilation strategy recommended by the ARDS Network. Such a redistribution pattern of pulmonary perfusion, which is illustrated in Figure 3, is compatible with lung recruitment [41].
Figure 3
Figure 3

Pulmonary perfusion maps of the left lung in one animal with acute lung injury induced by lavage. Left panel: Perfusion map after induction of injury and mechanical ventilation according to the ARDS Network protocol. Right panel: Perfusion map after 6 h of mechanical ventilation according to the ARDS Network protocol, but using variable tidal volumes. Note the increase in perfusion in the more dependent basal-dorsal zones (ellipses), suggesting alveolar recruitment through variable ventilation. Blue voxels represents lowest and red voxels, highest relative pulmonary blood flow. Adapted from [41].

The phenomenon of stochastic resonance may explain the higher efficiency of variable ventilation as a recruitment maneuver. In non-linear systems, like the respiratory system, the amplitude of the output can be modulated by the noise in the input. Typical inputs are driving pressure, VT, and respiratory rate, while outputs are the mechanical properties, lung volume, and gas exchange. Thus, by choosing appropriate levels of variability (noise) in VT during variable volume controlled ventilation, or in driving pressure during variable pressure controlled ventilation [48], the recruitment effect can be optimized.

Despite the considerable amount of evidence regarding the potential of variable ventilation to promote lung recruitment, this mechanism is probably less during assisted ventilation. In experimental ALI, we showed that noisy pressure support ventilation (noisy PSV) improved oxygenation [49, 50], but this effect was mainly related to lower mean airway pressures and redistribution of pulmonary blood flow towards better ventilated lung zones.

Conclusion

In patients with ALI/ARDS, considerable uncertainty remains regarding the appropriateness of recruitment maneuvers. The success/failure of such maneuvers may be related to the nature, phase, and/or extent of the lung injury, as well as to the specific recruitment technique. At present, the most commonly used recruitment maneuver is the conventional sustained inflation, which may be associated with marked respiratory and cardiovascular adverse effects. In order to minimize such adverse effects, a number of new recruitment maneuvers have been suggested to achieve lung volume expansion by taking into account the level and duration of the recruiting pressure and the pattern/frequency with which this pressure is applied to accomplish recruitment. Among the new types of recruitment maneuver, the following seem particularly interesting: 1) incremental increase in PEEP limiting the maximum inspiratory pressure; 2) pressure-controlled ventilation applied with escalating PEEP and constant driving pressure; 3) prolonged lower pressure recruitment maneuver with PEEP elevation up to 15 cmH2O and end-inspiratory pauses for 7 sec twice per minute during 15 min; 4) intermittent sighs to reach a specific plateau pressure in volume or pressure control mode; and 5) long slow increase in inspiratory pressure up to 40 cmH2O (RAMP). Moreover, the use of variable controlled ventilation, i.e., application of breath-by-breath variable VTs or driving pressures, as well as assisted ventilation modes such as Bi-Vent+PSV, may also prove a simple and interesting alternative for lung recruitment in the clinical scenario. Certainly, comparisons of different lung recruitment strategies and randomized studies to evaluate their impact on morbidity and mortality are warranted in patients with ALI/ARDS.

Abbreviations

ALI: 

acute lung injury

APCV: 

assist-pressure controlled ventilation

ARDS: 

acute respiratory distress syndrome

CT: 

computed tomography

PSV: 

pressure support ventilation

PEEP: 

positive end-expiratory pressure

PCIII: 

type III procollagen

Pplat: 

plateau pressure

VILI: 

ventilator-induced lung injury

VT: 

tidal volume.

Declarations

Authors’ Affiliations

(1)
Department of Ambient Health and Safety, Servizio Anestesia B, Ospedale di Circolo, University of Insubria, Viale Borri 57, 21100 Varese, Italy
(2)
Department of Anesthesiology and Intensive Care, Pulmonary Engineering Group, University Hospital Carl Gustav Carus, Fetscherstr. 74, 01307 Dresden, Germany
(3)
Laboratory of Pulmonary Investigation, Universidade Federal do Rio de Janeiro, Instituto de Biofisica Carlos Chagas Filho, C.C.S. Ilha do Fundao, 21941-902 Rio de Janeiro, Brazil

References

  1. Phua J, Badia JR, Adhikari NKJ, et al: Has mortality from acute respiratory distress syndrome decreased over time?. Am J Respir Crit Care Med. 2009, 179: 220-227. 10.1164/rccm.200805-722OC.View ArticlePubMedGoogle Scholar
  2. Oeckler RA, Hubmayr RD: Ventilator-associated lung injury: a search for better therapeutic targets. Eur Respir J. 2007, 30: 1216-1226. 10.1183/09031936.00104907.View ArticlePubMedGoogle Scholar
  3. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000, 342 (18): 1301-1308. 10.1056/NEJM200005043421801.View ArticleGoogle Scholar
  4. Pelosi P, Goldner M, McKibben A, et al: Recruitment and derecruitment during acute respiratory failure: an experimental study. Am J Respir Crit Care Med. 2001, 164: 122-130.View ArticlePubMedGoogle Scholar
  5. Pássaro CP, Silva PL, Rzezinski AF, et al: Pulmonary lesion induced by low and high positive end-expiratory pressure levels during protective ventilation in experimental acute lung injury. Crit Care Med. 2009, 37: 1011-1017. 10.1097/CCM.0b013e3181962d85.View ArticlePubMedGoogle Scholar
  6. Imai Y, Parodo J, Kajikawa O, et al: Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA. 2003, 289: 2104-2112. 10.1001/jama.289.16.2104.View ArticlePubMedGoogle Scholar
  7. Hodgson C, Keating JL, Holland AE, et al: Recruitment manoeuvres for adults with acute lung injury receiving mechanical ventilation. Cochrane Database Syst Rev. 2009, 15: CD006667-Google Scholar
  8. Fan E, Wilcox ME, Brower RG, et al: Recruitment maneuvers for acute lung injury: a systematic review. Am J Respir Crit Care Med. 2008, 178: 1156-1163. 10.1164/rccm.200802-335OC.View ArticlePubMedGoogle Scholar
  9. Maggiore SM, Lellouche F, Pigeot J, et al: Prevention of endotracheal suctioning-induced alveolar rerecruitment in acute lung injury. Am J Respir Crit Care Med. 2003, 167: 1215-1224. 10.1164/rccm.200203-195OC.View ArticlePubMedGoogle Scholar
  10. Martynowicz MA, Walters BJ, Hubmayr RD: Mechanisms of recruitment in oleic acidinjured lungs. J Appl Physiol. 2000, 90: 1744-1753.Google Scholar
  11. Tremblay LN, Slutsky AS: Ventilator-induced lung injury: from the bench to the bedside. Intensive Care Med. 2006, 32: 24-33. 10.1007/s00134-005-2817-8.View ArticlePubMedGoogle Scholar
  12. Gattinoni L, Pesenti A: The concept of "baby lung". Intensive Care Med. 2005, 31: 776-784. 10.1007/s00134-005-2627-z.View ArticlePubMedGoogle Scholar
  13. Cakar N, Akinci O, Tugrul S, et al: Recruitment maneuver: does it promote bacterial translocation?. Crit Care Med. 2002, 30: 2103-2106. 10.1097/00003246-200209000-00025.View ArticlePubMedGoogle Scholar
  14. Halbertsma FJ, Vaneker M, Pickkers P, et al: A single recruitment maneuver in ventilated critically ill children can translocate pulmonary cytokines into the circulation. J Crit Care. 2009Google Scholar
  15. Lim SC, Adams AB, Simonson DA, et al: Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury. Crit Care Med. 2004, 32: 2378-2384. 10.1097/01.CCM.0000147444.58070.72.View ArticlePubMedGoogle Scholar
  16. Rocco PRM, Pelosi P: Pulmonary and extrapulmonary acute respiratory distress syndrome: myth or reality?. Curr Opin Crit Care Med. 2008, 14: 50-55. 10.1097/MCC.0b013e3282f2405b.View ArticleGoogle Scholar
  17. Kloot TE, Blanch L, Youngblood MA, et al: Recruitment maneuvers in three experimental models of acute lung injury. Effect on lung volume and gas exchange. Am J Respir Crit Care Med. 2000, 161: 1485-1494.View ArticlePubMedGoogle Scholar
  18. Riva DR, Oliveira MB, Rzezinski AF, et al: Recruitment maneuver in pulmonary and extrapulmonary experimental acute lung injury. Crit Care Med. 2009, 36: 1900-1908. 10.1097/CCM.0b013e3181760e5d.View ArticleGoogle Scholar
  19. Wrigge H, Zinserling J, Muders T, et al: Electrical impedance tomography compared with thoracic computed tomography during a slow inflation maneuver in experimental models of lung injury. Crit Care Med. 2008, 36: 903-909. 10.1097/CCM.0B013E3181652EDD.View ArticlePubMedGoogle Scholar
  20. Grasso S, Stripoli T, Sacchi M, et al: Inhomogeneity of lung parenchyma during the open lung strategy: a computed tomography scan study. Am J Respir Crit Care Med. 2009, 180: 415-423. 10.1164/rccm.200901-0156OC.View ArticlePubMedGoogle Scholar
  21. Ornellas D, Santiago VR, Rzezinski AF, et al: Lung mechanical stress induced by recruitment maneuver in different degrees of acute lung injury [abstract]. Am J Respir Crit Care Med. 2009, 179: A3837-Google Scholar
  22. Mutoh T, Guest RJ, Lamm WJE, Albert RK: Prone position alters the effect of volume overload on regional pleural pressures and improves hypoxemia in pigs invivo. Am Rev Respir Dis. 1992, 146: 300-306.View ArticlePubMedGoogle Scholar
  23. Nakos G, Batistatou A, Galiatsou E, et al: Lung and 'end organ' injury due to mechanical ventilation in animals: comparison between the prone and supine positions. Crit Care. 2006, 10: R38-10.1186/cc4840.PubMed CentralView ArticlePubMedGoogle Scholar
  24. Broccard AF, Shapiro RS, Schmitz LL, Ravenscraft SA, Marini JJ: Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model of acute respiratory distress syndrome. Crit Care Med. 1997, 25: 16-27. 10.1097/00003246-199701000-00007.View ArticlePubMedGoogle Scholar
  25. Valenza F, Guglielmi M, Maffioletti M, et al: Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role?. Crit Care Med. 2005, 33: 361-367. 10.1097/01.CCM.0000150660.45376.7C.View ArticlePubMedGoogle Scholar
  26. Richter T, Bellami G, Scott Harris R, et al: Effect of prone position on regional shunt, aeration, and perfusion in experimental acute lung injury. Am J Respir Crit Care Med. 2005, 172: 480-487. 10.1164/rccm.200501-004OC.PubMed CentralView ArticlePubMedGoogle Scholar
  27. Santana MC, Garcia CS, Xisto DG, et al: Prone position prevents regional alveolar hyperinflation and mechanical stress and strain in mild experimental acute lung injury. Respir Physiol Neurobiol. 2009, 167: 181-188. 10.1016/j.resp.2009.04.006.View ArticlePubMedGoogle Scholar
  28. Cakar N, der Kloot TV, 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.View ArticlePubMedGoogle Scholar
  29. Farias LL, Faffe DS, Xisto DG, et al: Positive end-expiratory pressure prevents lung mechanical stress caused by recruitment/derecruitment. J Appl Physiol. 2005, 98: 53-61. 10.1152/japplphysiol.00118.2004.View ArticlePubMedGoogle Scholar
  30. Villagrá A, Ochagavía A, Vatua S, et al: Recruitment maneuvers during lung protective ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002, 165: 165-170.View ArticlePubMedGoogle Scholar
  31. Brower RG, Morris A, MacIntyre N, et al: 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: 2592-2597. 10.1097/01.CCM.0000057909.18362.F6.View ArticlePubMedGoogle Scholar
  32. Odenstedt H, Aneman A, Kárason S, Stenqvist O, Lundin S: Acute hemodynamic changes during lung recruitment in lavage and endotoxin-induced ALI. Intensive Care Med. 2005, 31: 112-120. 10.1007/s00134-004-2496-x.View ArticlePubMedGoogle Scholar
  33. Meade MO, Cook DJ, Griffith LE, et al: A study of the physiologic responses to a lung recruitment maneuver in acute lung injury and acute respiratory distress syndrome. Respir Care. 2008, 53: 1441-1449.PubMedGoogle Scholar
  34. Constantin JM, Cayot-Constantin S, Roszyk L, et al: Response to recruitment maneuver influences net alveolar fluid clearance in acute respiratory distress syndrome. Anesthesiology. 2007, 106: 944-951. 10.1097/01.anes.0000265153.17062.64.View ArticlePubMedGoogle Scholar
  35. Musch G, Harris RS, Vidal Melo MF, et al: Mechanism by which a sustained inflation can worsen oxygenation in acute lung injury. Anesthesiology. 2004, 100: 323-330. 10.1097/00000542-200402000-00022.View ArticlePubMedGoogle Scholar
  36. Rzezinski AF, Oliveira GP, Santiago VR, et al: Prolonged recruitment manoeuvre improves lung function with less utrastructural damage in experimental mild acute lung injury. Respir Physiol Neurobiol. 2009, 169: 271-281. 10.1016/j.resp.2009.10.002.View ArticlePubMedGoogle Scholar
  37. Odenstedt H, Lindgren S, Olegard C, et al: Slow moderate pressure recruitment maneuver minimizes negative circulatory and lung mechanic side effects: evaluation of recruitment maneuvers using electric impedance tomography. Intensive Care Med. 2005, 31: 1706-1714. 10.1007/s00134-005-2799-6.View ArticlePubMedGoogle Scholar
  38. Steimback PW, Oliveira GP, Rzezinksi AF, et al: Effects of frequency and inspiratory plateau pressure during recruitment manoeuvres on lung and distal organs in acute lung injury. Intensive Care Med. 2009, 35: 1120-1128. 10.1007/s00134-009-1439-y.View ArticlePubMedGoogle Scholar
  39. Saddy F, Oliveira GP, Garcia CS, et al: Assisted ventilation modes reduce the expression of lung inflammatory and fibrogenic mediators in a model of mild acute lung injury. Intensive Care Med. 2010Google Scholar
  40. Funk DJ, Graham MR, Girling LG, et al: A comparison of biologically variable ventilation to recruitment manoeuvres in a porcine model of acute lung injury. Respir Res. 2004, 5: 22-10.1186/1465-9921-5-22.PubMed CentralView ArticlePubMedGoogle Scholar
  41. Spieth PM, Carvalho AR, Pelosi P, et al: Variable tidal volumes improve lung protective ventilation strategies in experimental lung injury. Am J Respir Crit Care Med. 2009, 179: 684-693. 10.1164/rccm.200806-975OC.View ArticlePubMedGoogle Scholar
  42. Suki B, Barabási AL, Hantos Z, Peták F, Stanley HE: Avalanches and power-law behaviour in lung inflation. Nature. 1994, 368: 615-618. 10.1038/368615a0.View ArticlePubMedGoogle Scholar
  43. Mutch WAC, Harms S, Graham MR, Kowalski SE, Girling LG, Lefevre GR: Biologically variable or naturally noisy mechanical ventilation recruits atelectatic lung. Am J Respir Crit Care Med. 2000, 162: 319-323.View ArticlePubMedGoogle Scholar
  44. McMullen MC, Girling LG, Graham MR, Mutch WAC: Biologically variable ventilation improves oxygenation and respiratory mechanics during one-lung ventilation. Anesthesiology. 2006, 105: 91-97. 10.1097/00000542-200607000-00017.View ArticlePubMedGoogle Scholar
  45. Boker A, Haberman CJ, Girling L, et al: Variable ventilation improves perioperative lung function in patients undergoing abdominal aortic aneurysmectomy. Anesthesiology. 2004, 100: 608-616. 10.1097/00000542-200403000-00022.View ArticlePubMedGoogle Scholar
  46. Bellardine CL, Hoffman AM, Tsai L, Ingenito EP, Arold SP, Lutchen KR, Suki B: Comparison of variable and conventional ventilation in a sheep saline lavage lung injury model. Crit Care Med. 2006, 34: 439-445. 10.1097/01.CCM.0000196208.01682.87.View ArticlePubMedGoogle Scholar
  47. Thammanomai A, Hueser E, Majumdar A, Bartolák-Suki E, Suki B: Design of a new variable-ventilation method optimized for lung recruitment in mice. J Appl Physiol. 2008, 104: 1329-1340. 10.1152/japplphysiol.01002.2007.View ArticlePubMedGoogle Scholar
  48. Beda A, Spieth PM, Handzsuj T, et al: A novel adaptive control system for noisy pressure controlled ventilation: A numerical stimulation and bench test study. Intensive Care Med. 2010Google Scholar
  49. Gama de Abreu M, Spieth P, Pelosi P, et al: Noisy pressure support ventilation: A pilot study on a new assisted ventilation mode in experimental lung injury. Crit Care Med. 2008, 36: 818-827. 10.1097/01.CCM.0000299736.55039.3A.View ArticlePubMedGoogle Scholar
  50. Spieth P, Carvalho AR, Güldner A, Pelosi P, et al: Effects of different levels of pressure support variability in experimental lung injury. Anesthesiology. 2009, 110: 14-215.Google Scholar

Copyright

© Springer-Verlag Berlin Heidelberg 2010. 2010

This article is published under license to BioMed Central Ltd. This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law.

Advertisement