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  • Commentary
  • Open Access

Recruitment and retention of lung volume

Critical Care20027:9

  • Published:


Both a reduction in tidal volume and alveolar recruitment may be necessary to prevent ventilator-induced lung injury in the management of patients with acute respiratory distress syndrome. The lung collapse associated with endotracheal suctioning produces hypoxaemia, but it also causes de-recruitment, potentially aggravating lung injury. A study conducted by Dyhr and colleagues demonstrates the benefit of lung recruitment manoeuvres after suctioning, which help to improve oxygenation and restore lung volume more rapidly. Although this intervention appears safe and beneficial, the precise role of lung volume recruitment manoeuvres remains to be elucidated.


  • acute respiratory distress syndrome
  • atelectasis
  • mechanical ventilation
  • suctioning

One of the most common procedures performed in mechanically ventilated patients is that of endotracheal suctioning. Although most health care workers are aware of the potential risks associated with this procedure, including hypoxaemia and haemodynamic compromise, the potential effects on the pathophysiology of the injured lung are not usually highlighted. The recent literature on the mechanical ventilation of patients with acute respiratory distress syndrome (ARDS) stresses the importance of opening and maintaining the patency of lung units in order to prevent ventilator-associated lung injury. The report from Dyhr and coworkers [1] in the present issue provides an important practical insight into the de-recruitment caused by endotracheal suctioning, and the value of the lung recruitment manoeuvre in reversing these effects.

Since it became generally accepted that high tidal volumes and inflation pressures are injurious to the lungs [2], clinical trials in mechanical ventilation have emphasized pressure and volume limitation [3,4]. However, a potential adverse effect of reduced tidal volume ventilation is loss functional lung volume, with progressive atelectasis occurring over time [5]. This de-recruitment of lung not only exacerbates hypoxaemia but may also produce further alveolar damage [6]. In fact, it has been demonstrated that the repetitive opening and closing of alveoli that occurs during tidal ventilation may produce local inflammation, as well as the systemic release of cytokines in the blood, potentially producing multiorgan failure [7].

In the light of these effects of tidal volume limitation, an 'open lung' strategy for mechanical ventilation has been advocated in ARDS [8] to improve hypoxaemia and reduce ventilator-induced lung injury. Recruitment of the lung occurs during tidal ventilation, and sufficient positive end-expiratory pressure can be used to counterbalance the tendency for the alveoli to close. However, not all alveoli are recruited during tidal ventilation in the injured lung because of surface tension and adhesive forces, and higher pressures are needed to reopen collapsed airways [9]. Methods used to recruit the lung include sustained inflation manoeuvres, sighs, high-frequency oscillation and prone positioning [10,11]. A clinical trial of an 'open lung' approach in patients with ARDS demonstrated a benefit over a 'conventional' ventilatory strategy that did not employ pressure limitation or lung volume recruitment [12].

The sustained inflation lung recruitment manoeuvre is a relatively simple and safe intervention for achieving lung volume recruitment [13]. Not all patients with ARDS demonstrate a recruitment response; those at an earlier stage in their disease and with normal chest wall mechanics derive most benefit [14]. Furthermore, the degree of 'recruitable' lung may vary with disease state. Although the patient with pneumonic consolidation may meet clinical criteria for ARDS (bilateral infiltrates and hypoxaemia), the pathophysiologies of the two states clearly differ. The loss of alveoli in pneumonia is due to consolidation rather than atelectasis from surfactant loss, and is less likely to be recruitable [11].

The small randomized controlled study conducted by Dyhr and colleagues provides clinical evidence of the significant loss of lung volume after endotracheal suctioning and the beneficial effect of a sustained inflation recruitment manoeuvre [1]. The eight patients studied had moderately severe ARDS (lung injury score 2.3–3.3) and were studied early in the course of their disease (they had been ventilated for <7 days). Half of the patients had a 'primary' cause of ARDS (i.e. pneumonia), which may be less responsive to recruitment attempts. Nevertheless, in the group as a whole the manoeuvre was effective in improving oxygenation, lung volume and respiratory system compliance more rapidly than did tidal ventilation and positive end-expiratory pressure alone. Lung recruitment following suctioning appears to be a more physiologically appropriate intervention than the usual approach of providing 100% oxygen during the procedure. In fact, this high inspired oxygen concentration may be counterproductive, tending to produce absorption atelectasis [15].

Although lung volume recruitment manoeuvres have a role to play in ventilatory management of patients with ARDS, this cannot be extrapolated to patients with other lung conditions. Many questions related to this intervention remain unanswered. Do recruitment manoeuvres actually open previously closed lung units? What is the optimal method and frequency for recruitment? Does this intervention improve outcome? A multicentre Canadian randomized clinical trial comparing a pressure limited strategy with and without an 'open lung' approach is currently in progress. The 'open lung' protocol includes lung recruitment manoeuvres after endotracheal suctioning and ventilator disconnects [16]. With this and other studies, the precise value of this intervention may become more clearly defined over the next few years.



= acute respiratory distress syndrome.


Authors’ Affiliations

Associate Director, Intensive Care Unit, Mount Sinai Hospital & Interdisciplinary Division of Critical Care, University of Toronto, Toronto, Ontario, Canada


  1. Dyhr T, Bonde J, Larsson A: Lung recruitment maneuvers are effective to regain lung volume and oxygenation after open endotracheal suctioning in acute respiratory distress syndrome. Critical Care 2003, in press.Google Scholar
  2. Slutsky AS: Mechanical ventilation. American College of Chest Physicians' Consensus. Chest 1993, 104: 1833-1859.View ArticlePubMedGoogle Scholar
  3. Stewart TE, Meade MO, Cook DJ, Granton JT, Hodder RV, Lapinsky SE, Mazer CD, McLean RF, Rogovein TE, Schouten BD, Todd TR, Slutsky AS: Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. N Engl J Med 1998, 338: 355-361. 10.1056/NEJM199802053380603View ArticlePubMedGoogle Scholar
  4. 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. 10.1056/NEJM200005043421801View ArticleGoogle Scholar
  5. Richard JC, Maggiore SM, Jonson B, Mancebo J, Lemaire F, Brochard L: 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.View ArticlePubMedGoogle Scholar
  6. Muscedere JG, Mullen JB, Gan K, Slutsky AS: Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994, 149: 1327-1334.View ArticlePubMedGoogle Scholar
  7. Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, Bruno F, Slutsky AS: Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA 1999, 282: 54-61. 10.1001/jama.282.1.54View ArticlePubMedGoogle Scholar
  8. Lachmann B: Open up the lung and keep the lung open. Intensive Care Med 1992, 18: 319-321.View ArticlePubMedGoogle Scholar
  9. Crotti S, Mascheroni D, Caironi P, Pelosi P, Ronzoni G, Mondino M, Marini JJ, Gattinoni L: Recruitment and derecruitment during acute respiratory failure. Am J Respir Crit Care Med 2001, 164: 131-140.View ArticlePubMedGoogle Scholar
  10. Mehta S: Lung volume recruitment. Curr Opin Crit Care 1998, 4: 6-15.View ArticleGoogle Scholar
  11. Pelosi P, Cadringher P, Bottino N, Panigada M, Carrieri F, Riva E, LIssoni A, Gattinoni L: Sigh in acute respiratory distress syndrome. Am J Respir Crit Care 1999, 159: 872-880.View ArticleGoogle Scholar
  12. Amato MBP, Barbas CSV, Medeiros DM, Magaldi RB, Schettino GB, Lorenzi-Filho G, Kairalla RA, Deheinzelin D, Munoz C, Oliveira R, Takagaki TY, Carvalho CR: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998, 338: 347-354. 10.1056/NEJM199802053380602View ArticlePubMedGoogle Scholar
  13. Lapinsky SE, Aubin M, Mehta S, Boiteau P, Slutsky AS: Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intensive Care Med 1999, 25: 1297-1301.View ArticlePubMedGoogle Scholar
  14. Grasso S, Mascia L, Del Turco M, Malacarne P, Giunta F, Brochard L, Slutsky AS, Ranieri M: Effects of recruiting maneuvers in patients with acute respiratory distress syndrome ventilated with protective strategy. Anesthesiology 2002, 96: 795-802.View ArticlePubMedGoogle Scholar
  15. Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstierna G: Influence of gas composition on recurrence of atelectasis after a reexpansion manoeuvre. Anesthesiology 1995, 82: 832-842. 10.1097/00000542-199504000-00004View ArticlePubMedGoogle Scholar
  16. Stewart TE, Meade MO, Slutsky AS, Hand L, Ronco J, Chittock D, Evans D, Hodder R, Griffith L, Graham J, Lessard M, Magder S, Laporta D: Complications of a lung recruitment maneuver [abstract]. Am J Respir Crit Care Med 2002, 165: A682.Google Scholar


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