Recruitment maneuvers and other strategies in the use of mechanical ventilation, which can both save and harm lives, might be a factor in recently decreasing mortality rates.
The adult respiratory distress syndrome (ARDS) is described as a clinical syndrome associated with respiratory distress of acute onset, refractory hypoxemia, decreased respiratory-system compliance, and diffuse pulmonary infiltrates visible on a chest radiograph. The mortality rate differs greatly between centers, but generally approximates 50%. Fortunately, there are some data showing that mortality has been decreasing over recent years. As therapy for ARDS is largely supportive, it is not possible to identify a specific factor causing this improvement. Nevertheless, ventilation strategy is the factor that has changed to a great extent over the past decade.
Ventilator-Induced Lung Injury
On the one hand, mechanical ventilation is a lifesaving procedure, as it keeps the body adequately oxygenated. On the other hand, the same procedure has the potential to bring harm to the patient. The traditional approach to mechanical ventilation, used in anesthesiology and intensive care for many years, used high tidal volumes (Vt) of 10 to 15 mL/kg and insisted on normocapnia and adequate oxygenation. More recently, it has been hypothesized that large tidal volumes with low positive end-expiratory pressure (PEEP) might be hazardous and might lead to alveolar damage. Animal experiments1-3 have shown the classic approach to cause ventilator-induced lung injury. This syndrome is typically characterized by increased alveolocapillary-membrane permeability, high-protein content edema, surfactant failure, and decreased pulmonary compliance. Patients with ARDS often need high inspiratory airway pressures because of these pathophysiological characteristics. Histopathological changes of the lung are heterogeneous,4 with edematous and consolidated areas coexisting with relatively normal regions. High airway pressures, applied to healthy regions, present the risk of overdistension and subsequent alveolar injury; however, the precise mechanism of damage is not known. Peak airway pressures, PEEP levels, and repetitive opening and closing of alveolar units have been proposed as responsible.
Information is now available to prove that inappropriate mechanical ventilation could even activate cytokine production in the lung.5 Elevation of pulmonary cytokines, together with the inadequacy of the alveolocapillary membrane, may result in the involvement of extrapulmonary organs, leading to multiple organ failure.6 Stüber et al7 demonstrated that mechanical ventilation with low PEEP and high Vt induces release of proinflammatory and anti-inflammatory cytokines into the alveolar space and the blood after only 1 hour. Lung-protective ventilation is able to reverse this systemic inflammatory response.
Protective Ventilation Strategy
Decreasing Vt could reduce the risk of ventilator-induced lung injury, so small-Vt ventilation has been studied extensively.8-12 The ARDS Network study9 compared the traditional strategy using a Vt of 12 mL/kg predictive body weight with a lower Vt of 6 mL/kg. Despite some difficulties encountered in comparing the trials involved, the ARDS Network study, in contrast with other randomized clinical trials,10-12 demonstrated improved clinical outcomes for the low-Vt strategy. In a study by Amato et al,13 conventional mechanical ventilation was compared with protective ventilation strategy. Improved survival was found for the latter. Brochard et al10 did not find a similar benefit.
Unfortunately, reducing Vt involves the potential to produce atelectasis and the cyclic opening and closing of some unstable lung regions. Transpulmonary pressures accompanying repetitive opening and closing of those lung units can reach extremely high levels that can cause microtrauma to the alveolocapillary membrane.14 Protective ventilation strategy focuses on the use of a small Vt and on recruitment maneuvers with adequate PEEP to open alveoli, and keep them open, at a safe level. This prevents additional lung damage from alveolar overdistension and shear stress due to collapse and cyclic rerecruitment and derecruitment.
Lung opening has been thought to occur primarily around the lower inflection point of the pressure-volume curve or within a narrow range.15 Some authors16,17 have stated that only the presence of a lower inflection point on the pulmonary pressure-volume curve means that there is a potential for the recruitment of previously collapsed lung regions without an inappropriate risk of overinflation. Gattinoni et al18 showed, however, that continuous recruitment occurs during insufflation from 0 to 30 cm H2O. They and others19,20 support the theory that lung recruitment happens far above the lower inflection point and probably takes place along the entire pressure-volume curve.
The use of the pressure-volume curve as a tool for setting ventilatory strategy in patients with ARDS is often criticized. The lower inflection point can be related either to lung parenchymal compliance or to the chest walls elastic properties. In many patients, no lower inflection point can be identified. Its measurement is technically difficult, and poor physician-to-physician correlation in its determination has been shown.21 Consequently, we do not routinely use pressure-volumecurve measurement in our daily praxis at St Ann´s University Hospital, Brno, Czech Republic.
There is currently no exact guideline in the medical literature for performing a recruitment maneuver; centers differ greatly in the techniques used. The widely accepted, standard method is the use of sustained inflation with continuous positive airway pressure (CPAP). Once collapsed, lung tissueswhether healthy or injuredrequire extremely high airway pressures to recruit. In a porcine model of ARDS, Sjöstrand et al22 needed to use peak airway pressures as high as 55 cm H2O, maintained for 5 to 10 minutes, to open the lung. Amato et al15 applied 35 to 40 cm H2O of CPAP for 30 to 40 seconds and Lapinsky et al23 used 30 to 45 cm H2O for 20 seconds multiple times to recruit collapsed lung areas. Gattinoni et al24 reported the need for a pressure of 46 cm H2O to open atelectasis in patients with ARDS. Rothen et al24 had previously studied healthy patients during anesthesia; they found that a pressure of 40 cm H2O, held for 15 seconds, was required to recruit lung atelectasis after 20 minutes of general anesthesia.
Pressures of about 40 cm H2O were arbitrarily accepted as the baseline level for recruitment maneuvers. In conditions characterized by chest-wall restriction (such as abdominal sepsis), higher pressures may be necessary to achieve sufficient transalveolar pressure.25
Periodic use of deep breaths or sighs has also been suggested for lung recruitment. Pelosi et al26 used a set of sighs consisting of high Vt to reach a 45 cm H2O plateau pressure in volume-control ventilation.
Byford et al27 advocated the use of small fluctuations in Vt added to CPAP during high-frequency ventilation as more effective in recruiting lung volumes than CPAP alone in rabbits.
There are three major kinds of recruitment maneuver: CPAP alone for a sufficient time, sustained inflation for a sufficient time with or without small Vt, and sighing using high airway pressures with high Vt. All three represent the same general principle. Further comparative studies evaluating the differences in their efficacy and safety are needed.
In our clinical praxis, recruitment maneuvers using sustained inflation with small tidal volumes seem to be superior to simple sustained inflation. We do not change the fraction of inspired oxygen if the pulse oximetry result (Spo2) is acceptable (>88%). PEEP is set at 40 cm H2O, and we use additional peak airway pressures, 5 to 10 cm H2O above PEEP, for 15 to 30 breaths. PEEP is decreased, stepwise, to reach a Vt of 6 mL/kg. Keeping the driving pressure (peak pressure minus PEEP) constant, we decrease PEEP in increments of 1 to 2 cm H2O. We find the closing pressure by looking for a sudden decrease in oxygenation or a disproportional decrease in Vt. We then repeat this process, but we stop reducing PEEP 2 cm H2O above the closing pressure that we have determined.
We terminate the maneuver prematurely if hypotension occurs (if mean arterial pressure decreases 30%) or if Spo2 drops below 88% (or by 5%). We use heavy sedation without muscle relaxants.
It is evident from clinical observations that opening the lung for a limited period is not sufficient to prevent derecruitment.25 Repetitive maneuvers must be performed, but their ideal frequency is unclear. We rarely use recruitment maneuvers more than twice per day.
It has been shown that ARDS due to a direct insult (pneumonia) has different characteristics and a lower potential for recruitment than ARDS having an extrapulmonary origin (such as abdominal sepsis).26,28
Positioning and Monitoring
The prone position is an adjunct to lung-protective ventilation that promotes lung recruitment. In an animal study, Cakar et al29 compared two groups of recruitment maneuvers performed in either supine or prone positions. The recruitment maneuvers performed in the prone position were more effective. Based on this idea, some centers (unlike our department) apply maneuvers entirely in the prone position. We use open lung maneuvers independently of patients position as we see its adequate effectiveness in supine as well.
The most important tool for checking the effectiveness of recruitment maneuvers is probably the CT scan.30 Unfortunately, the need to transport severely diseased patients makes CT imaging impractical for everyday use where bedside CT is unavailable. Bedside measurements of compliance may be totally misleading and disappointing. Continuous arterial blood gas monitoring may be worthwhile, but can be expensive. We routinely use pulse oximetry, intermittent blood-gas analysis, standard ventilator monitoring, invasive blood-pressure measurement, and portable (bedside) chest radiography.
Unfortunately, recruitment maneuvers are not without hazards. An extremely careful approach to lung-opening strategies is mandatory in patients with chronic obstructive pulmonary disease and after pulmonary resection. We can report that one patient developed severe ARDS following scheduled lobectomy due to neoplasia; repeated recruitment maneuvers with relatively low peak pressures were applied, but a persistent bronchopleural fistula with a significant air leak developed.
Transient hypotension, bradycardia,23 and decreased gastric mucosal blood flow have also been reported.31
Recruitment maneuvers are suggested as an important component of ARDS ventilatory strategy. If administered carefully, recruitment maneuvers can improve oxygenation without inappropriate risk. Although recruitment maneuvers have been studied extensively, there is no evidence-based recommendation covering which recruitment maneuvers should be used and how often they should be performed.
Martin Pavlík, MD, EDAD, and V. Zvonícek, MD, are assistant professors in the Department of Anesthesia and Intensive Care, Saint Ann´s University Hospital, Brno, Czech Republic.
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