Clinical review: the implications of experimental and clinical studies of recruitment maneuvers in acute lung injury

Abstract

Mechanical ventilation can cause and perpetuate lung injury if alveolar overdistension, cyclic collapse, and reopening of alveolar units occur. The use of low tidal volume and limited airway pressure has improved survival in patients with acute lung injury or acute respiratory distress syndrome. The use of recruitment maneuvers has been proposed as an adjunct to mechanical ventilation to re-expand collapsed lung tissue. Many investigators have studied the benefits of recruitment maneuvers in healthy anesthetized patients and in patients ventilated with low positive end-expiratory pressure. However, it is unclear whether recruitment maneuvers are useful when patients with acute lung injury or acute respiratory distress syndrome are ventilated with high positive end-expiratory pressure, and in the presence of lung fibrosis or a stiff chest wall. Moreover, it is unclear whether the use of high airway pressures during recruitment maneuvers can cause bacterial translocation. This article reviews the intrinsic mechanisms of mechanical stress, the controversy regarding clinical use of recruitment maneuvers, and the interactions between lung infection and application of high intrathoracic pressures.

Figure 1

Dynamic loops during three modes of ventilation inscribed into the quasistatic pressure–volume curve of the respiratory system of an animal after lung washes. Loop A: tidal insuflation with a positive end-expiratory pressure (PEEP) below the lower inflection point before a sustained inflation. Loop B: tidal insuflation with a PEEP below the lower inflection point after a sustained inflation. Loop C: PEEP higher than the lower inflection point after a sustained inflation. Sustained inflation promoted alveolar recruitment at low PEEP levels (loop B). Sustained inflation superimposed on high PEEP favored alveolar overdistension in this model of surfactant depletion (loop C). Reproduced with permission from Rimensberger and coworkers [16].

Figure 2

Relationship between recruitment maneuver (RM)-induced changes in arterial oxygen tension (PaO₂)/fractional inspired oxygen (FiO₂) and RM-induced changes in pulmonary shunt (Qva/Qt). A significant negative correlation was found between these two parameters (r = -0.85; P < 0.01). In these patients with acute respiratory distress syndrome (ARDS), who were near optimally recruited by positive end-expiratory pressure and tidal volume, the addition of a RM induced alveolar overdistension with redistribution of blood flow and consequently an increase in intrapulmonary shunt. Responders: solid circles; nonresponders: solid triangles. Reproduced and modified with permission from reference Villagrá and coworkers [33].

Figure 3

Physiologic variables in a representative nonresponder and in a responder acute respiratory distress syndrome (ARDS) patient before, during, and after recruitment maneuvers (RMs). In patients with a stiff chest wall (nonresponders) the degree of airway pressure transmitted to the pleural space was greater. Subsequently, during the RM, the transpulmonary pressure and the change in lung volume were lower. The reduction in blood pressure was higher in nonresponders than in patients with normal chest wall (responders). From top to bottom: flow, airway opening pressure (Pao), and changes in lung volume (ΔV), esophageal pressure (ΔPes), transpulmonary pressure (P_L), arterial blood pressure (ABP), and right atrial pressure (RAP) with worsening hemodynamics. Reproduced and modified with permission from Grasso and coworkers [38].