Special Feature

Recruitment Maneuvers in ARDS

By Enrique Piacentini, MD, and Francisco Baigorri, MD, PhD

Mechanical ventilation (MV) is a supportive life-saving therapy in patients with acute respiratory distress syndrome (ARDS). In the last decade, the possibility that MV can produce alterations in lungs, namely ventilator-induced lung injury, has been recognized.1 To minimize this damage, lung protective strategies to avoid the overdistension and cyclic collapse and re-opening of alveoli have been successfully used in patients with ARDS receiving MV.2,3 Recruitment maneuvers (RM) consisting of sustained inflation to open the collapsed alveolar units have been proposed as an adjunct in the ventilatory management of patients with ARDS.4,5 However, in most instances, lung recruitment and overdistension occur simultaneously at higher intrathoracic pressure than when RM are not used.6 Moreover, whether the effect of RM on healthy parts of the lung might induce triggering of cellular mechanisms of injury is still unknown. The objective of this essay is to briefly review the implications of experimental and clinical studies of RM in ARDS patients.

Experimental Evidence on Recruitment Maneuvers

The beneficial effects of RM have been demonstrated in animal models of alveolar collapse induced by surfactant depletion, such as saline-lavaged rabbit lungs. In this model, an improvement in respiratory system compliance and oxygenation were observed after RM.7 However, some data suggest that RM have different effects depending on the type of lung insult and also on the use of different combinations of tidal volume and positive end-expiratory pressure (PEEP). Whether RM are necessary to prevent alveolar collapse when optimal PEEP is used remains controversial. Van der Kloot and colleagues8 studied the effects of RM on gas exchange and lung volumes in 3 experimental models of acute lung injury: saline lavage, oleic acid infusion, and induced pneumonia. After RM, oxygenation improved only in the surfactant-depletion group when low PEEP was used. At high PEEP, RM had no effect in any of the ARDS models tested.9

Recruitment Maneuvers in ARDS Patients

Since the reports of Amato and associates2 and the Consensus Conference on ARDS,10 the application of periodic RM in patients with ARDS has gained acceptance among clinicians—although controversy still remains. Recruitment improved oxygenation, intrapulmonary shunt, and lung mechanics, but these effects were lost when the patients were ventilated with high PEEP, suggesting that high PEEP better stabilized alveoli and prevented lung volume loss. In the same line, beneficial effects on oxygenation were observed, but only if PEEP was increased after RM.11,12

Other studies have shown a modest and variable effect of RM on oxygenation when ARDS patients are ventilated with high PEEP. Richard and colleagues13 demonstrated decreased oxygenation when tidal volume was decreased from 10 mL/kg to 6 mL/kg with PEEP set above the lower inflection point of the pressure-volume curve. However, increasing PEEP and RM prevented alveolar derecruitment, and RM performed in patients already ventilated with high PEEP had minimal effects on requirements for oxygenation support. Similarly, Villagrá and associates,14 studying the effect of RM superimposed on a lung-protective strategy, found no effect on oxygenation regardless of the stage of ARDS; furthermore, in some patients, venous admixture increased during RM.

In summary, RM can be useful to improve oxygenation in patients receiving MV with low levels of PEEP and low tidal volumes. However, in patients with ARDS receiving MV with high PEEP levels, the beneficial effects of RM were not observed.

Lung Infection and Mechanical Ventilation

Recent studies suggest that the detrimental effect of MV can be aggravated when lungs are infected or primed with endotoxin. Experimental studies demonstrated the strong effect of both MV and infection on the lung because they seem to act synergistically when causing alveolar damage.15 These experimental studies suggest that for a similar lung infection, the presence of MV (cyclic positive intrathoracic pressure) favors greater bacterial burden and enhanced bacterial translocation from the lung into systemic circulation. These effects are particularly important when using ventilatory strategies that apply large transpulmonary pressures (high tidal volume and/or high alveolar pressures without PEEP)16 and are partially attenuated when lung-protective ventilatory strategies are used.17 Recruitment maneuvers appear to exert little effect on consolidated lung areas but can cause overdistension in some lung regions where bacteria are compartmentalized on the site of infection or colonization.


Considerable uncertainty remains regarding the use of RM in humans with ARDS. RM may have a role in patients with early ARDS and normal chest wall mechanics since there is great potential for alveolar recruitment, and after disconnections from the ventilator where sudden loss of lung volume promotes alveolar instability and derecruitment. Recommendations to use RM as adjuncts during lung protection ventilatory strategies seem unnecessary since sustained improvements in lung function have not been found when both strategies are combined. The presence of lung infection must be considered a major limitation for aggressive RM since translocation of bacteria and occurrence of systemic sepsis have been demonstrated in animal models. Ultimately, then, the use of RM cannot be recommended, and if used, RM should be restricted to an individualized clinical decision or as a last resort to improve oxygenation and lung mechanics in a severely hypoxemic ARDS patient.


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2. Amato MBP, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338:347-354.

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;342:1301-1308.

4. Rothen HU, et al. Dynamics of re-expansion of atelectasis during general anesthesia. Br J Anaesth. 1999; 82:551-556.

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7. Rismensberger PC, et al. The open lung during small tidal volume ventilation: Concepts of recruitment and "optimal" positive end-expiratory pressure. Crit Care Med. 1999;27:1946-1952.

8. Van der Kloot TE, 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.

9. Fujino Y, et al. Repetitive high-pressure recruitment maneuvers required to maximally recruit lung in sheep model of acute respiratory distress syndrome. Crit Care Med. 2001;29:1579-1586.

10. Artigas A, et al. The American-European Consensus Conference on ARDS, part 2. Ventilatory, pharmacologic, supportive therapy, study design strategies and issues related to recovery and remodeling. Intensive Care Med. 1998;24:378-398.

11. Lapinsky SE, et al. Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intensive Care Med. 1999;25:1297-1301.

12. Lim CM, et al. 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.

13. Richard JC, et al. Influence of tidal volume on alveolar recruitment. Respective role of PEEP and a recruitment maneuver. Am J Respir Crit Care Med. 2001; 163:1609-1613.

14. Villagrá A, et al. Recruitment maneuvers during lung protective ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002;165:165-170.

15. Charles PE, et al. New model of ventilator-associated pneumonia in immunocompetent rabbits. Crit Care Med. 2002;10:2278-2283.

16. Nahum A, et al. Effect of mechanical ventilation strategy on dissemination of intratracheally instilled Escherichia coli in dogs. Crit Care Med. 1997;10: 1733-1743.

17. Savel RH, et al. Protective effects of low tidal volume ventilation in a rabbit model of Pseudomonas aeruginosa-induced acute lung injury. Crit Care Med. 2001;2:392-398.

Dr. Piacentini is a Research Fellow, Critical Care Centre, Hospital de Sabadell, Institut Universitari Parc Taulí, Universitat Autònoma de Barcelona, Sabadell, Spain.