A recruitment maneuver (RM) is the process of inducing an intentional transient increase in transpulmonary pressure aimed at reopening non-aerated or poorly aerated alveoli. The immediate expected benefits are improvements in oxygenation and respiratory system compliance [1].

During an RM the transpulmonary pressure should overcome the critical opening pressure of at least a substantial proportion of closed alveoli. Once these alveoli are re-opened, pressure needed to avoid re-collapse is lower because during deflation a greater lung volume is achieved at a certain pressure level (Fig. 1a). The difference between pressure–volume (P–V) curves during inflation and deflation is the hysteresis. Thus, as long as positive end-expiratory pressure (PEEP) is kept above a critical pressure level, recruited alveoli will remain opened [1].

Fig. 1
figure 1

Pressure–volume curve (a). During inflation (full line) transpulmonary pressure overcomes the critical opening pressure (upper inflection point). After recruitment maneuver, during deflation (dotted line), lung volume is greater at a certain pressure level, and alveoli remain opened as long as positive end-expiratory pressure (PEEP) is kept above a critical pressure level (lower inflection point). Pressure–time (seconds) curve (b) showing a sustained inflation recruitment maneuver using continuous positive airway pressure (CPAP) of 40 cmH2O for 40 s. Pressure–time (minutes) curve showing a stepwise recruitment maneuver (c) using both inspiratory pressure and PEEP increases, keeping driving pressure fixed at 15 cmH2O, achieving peak pressure after recruitment of 50 cmH2O and PEEP of 35 cmH2O. After recruitment, figure shows a decremental PEEP titration and a new recruitment maneuver performed after an optimal PEEP is identified (i.e., the PEEP associated with best compliance of respiratory system or best oxygenation). After the new recruitment, PEEP is set 2 cmH2O above the optimal level

Full size image

A series of patients with early acute respiratory distress syndrome (ARDS) receiving RM monitored by tomography showed that with zero end-expiratory pressure (ZEEP) there is a huge amount of collapsed alveoli at the gravitational-dependent lung zones [2]. With PEEP set 2 cmH2O above the critical opening pressure, 20–30 % of the lung is still collapsed [2]. After RM achieving plateau pressures as high as 55 or 60 cmH2O, less than 5 % of the total lung mass remains collapsed. The lungs showed less alveolar collapse on the deflation limb of the P–V curve (after RMs) when equivalent pressures were applied during the inflation (Fig. 1a).

The effect of RMs on oxygenation is marked [2, 3], thus RMs have a clear role as rescue therapy for patients with severe hypoxemia, refractory to protective ventilation strategies and prone position. Indeed, the LOV Study compared ventilation strategy including RM plus higher levels of PEEP to a control strategy with no recruitment and lower PEEP levels and showed decreased risk of death due to refractory hypoxemia in the experimental group [4]. It is important to note that most studies with RMs not followed by titrated PEEP observed rapid decline in PaO2/FiO2 [5]. Conversely, in patients ventilated with an optimal titrated PEEP after the RM, the oxygenation gains were sustained for days [2, 3].

Response to RMs is not homogenous in ARDS patients [6]. ARDS-associated fibroproliferation is more prevalent in late ARDS and may impair response to RMs; thus, although clear time cutoffs have not been established, these maneuvers are unlikely to benefit patients with more than 5 days of ARDS [7]. Other factors associated with poorer response to RMs are more focal as opposed to diffuse morphology [8], higher PaO2/FiO2 ratios and respiratory-system compliance, and lower levels of dead space [6].

Although RMs are useful for improving oxygenation, only a few patients with ARDS die because of refractory hypoxemia [4]. Thus, a more relevant question is whether RMs may improve ventilator-induced lung injury (VILI) and clinical outcomes. The two independent main mechanisms of VILI are overdistention and atelectrauma, which is local shear injury attributed to cyclic opening and closing of distal small airways and alveoli [9].

Ventilation strategies using low tidal volumes but also low PEEP levels such as the ARDSNet protocol aim to prevent VILI by overdistention. However, this approach may lead to substantial cyclic opening and closing of alveolar units with worsening of VILI [9]. Positron emission tomography studies of experimental models of ARDS revealed that early inflammation is more pronounced in intermediate gravitational zones corresponding to normally or poorly aerated regions, as opposed to posterior collapsed or anterior overdistended zones [10]. These findings suggest that tidal stretch is a major mechanism in VILI. Indeed, experimental models of ARDS have shown that keeping higher PEEP levels may decrease further lung damage even when animals were ventilated at lower tidal volumes [9].

Alveolar fluid clearance is also impaired in most patients with ARDS [11]. Inhibition of fluid clearance is probably caused by hypoxia and by injured alveolar epithelium with disrupted cells. RMs may decrease lung edema, possibly by improving oxygenation and decreasing VILI [12].

Markers of inflammation and of alveolar epithelial type I cell injury decrease after RM and PEEP titration in ARDS [3, 13]. In addition, by re-opening collapsed alveoli, RMs can also increase respiratory system compliance and, as a consequence, reduce driving pressure which is the pressure needed to deliver a given tidal volume [14]. Finally, the reduction in driving pressure may ultimately improve survival of patients with ARDS [14].

Many RM techniques have been described, including sighs, sustained inflation, stepwise increase of inspiratory pressure and/or of PEEP. Intermittent sighs involves increasing tidal volume or level of PEEP for one of several breaths. Effectiveness of sighs is short-lived and they may lead to increased levels of inflammation markers [15]. Sustained inflation is the most commonly investigated method and involves use of continuous positive airway pressure (CPAP) of 40 cmH2O for about 40 s (Fig. 1b) [5]. Compared with sustained inflation, methods involving stepwise increases in pressures lead to less hemodynamic compromise and less microscopic and biochemical signs of lung injury [16]. Furthermore, the best results in terms of recruitability have been obtained with stepwise increases in PEEP up to 45 cmH2O with driving pressure fixed at 15 cmH2O (Fig. 1c) [2].

RMs may be performed in supine or prone position. In the later case, RMs and prone position have additive effects on oxygenation and respiratory system compliance. This is important, since the use of prone positioning has become the standard of care for patients with ARDS and PaO2/FiO2 ≤150 mmHg [17].

Although there is no standardization regarding the method to adjust PEEP after RMs, some method should be employed to identify a PEEP level capable of avoiding new collapse. A valuable bedside method, which does not require imaging, is decremental PEEP titration according to the best dynamic or static compliance [1]. Once the optimal PEEP is identified, lungs are recruited again, and PEEP is set 2 cmH2O above the optimal level [1].

The effects of RMs on clinical outcomes have been assessed in a meta-analysis of ten randomized trials, which suggested that RMs may reduce hospital mortality without increasing the risk of barotrauma in patients with moderate or severe ARDS [18]. However, our confidence in the estimate of effect is low, especially because most trials are at high risk of bias. Another systematic review found that the common adverse events after RM are hypotension, acidosis, and desaturation, but they are usually self-limited and without serious sequelae [5].

In summary, there is uncertainty regarding the clinical effectiveness of RMs to improve clinical outcomes of ARDS patients. Ongoing multicenter randomized trials should provide a reliable answer to this question. Therefore, although there is a role for RMs as a rescue therapy in refractory hypoxemia in patients with moderate to severe ARDS, there is currently no solid basis for their routine use in other patients.