Elsevier

Clinics in Chest Medicine

Volume 27, Issue 4, December 2006, Pages 601-613
Clinics in Chest Medicine

Conventional Mechanical Ventilation in Acute Lung Injury and Acute Respiratory Distress Syndrome

https://doi.org/10.1016/j.ccm.2006.06.009Get rights and content

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Ventilator-induced lung injury

Use of invasive mechanical ventilation for ARDS is problematic given the potential for VILI. VILI is a spectrum of injury that traditionally has been associated with the concepts of oxygen toxicity and macro-barotrauma (eg, lung rupture with subcutaneous emphysema, pneumothorax, pneumomediastinum, other forms of air leak). In actuality, macro-barotrauma is uncommon with contemporary ventilator approaches [2], [3], and the role of oxygen toxicity in humans remains controversial [4], [5].

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Volutrauma and the selection of tidal volume

Volutrauma, which results from large tidal volumes, leads to increased wall stress (“stretch”) of aerated alveoli, thereby causing parenchymal injury from either gross physical disruption of lung tissue or activation of stretch-responsive inflammatory pathways in lung epithelial cells. Inflammation and increased alveolar-capillary permeability result. Numerous experimental animal models of ARDS have shown that large tidal volumes lead to pulmonary epithelial and endothelial damage in normal

Atelectrauma and the selection of positive end-expiratory pressure

The deleterious effects of atelectrauma may result from cyclic closing and reopening of alveoli with each tidal breath, which leads to alveolar shear stress–related injury. Thus, atelectrauma is important to consider, especially given the heterogeneous nature of lung aeration in ALI/ARDS. Prevention of atelectrauma involves use of PEEP, recruitment maneuvers, or prone positioning. Proponents of the open-lung approach have advocated use of recruitment maneuvers to open previously closed alveoli

Is there a safe level of end-inspiratory alveolar pressure?

It has been proposed that airway plateau pressures lower than 30 to 32 cm H2O are safe. This belief stems from the observations that (1) transpulmonary pressures in normal, relaxed individuals at total lung capacity approximate these values, and (2) pre-ARDSNet tidal volume trials did not show benefit of tidal volume reduction when plateau airway pressures were below 32 cm H2O in both study cohorts [15], [32]. Experimental models, however, suggest that in injured lungs VILI may occur at airway

Hypercapnia

Hypercapnia is not a goal of lung-protective ventilation strategies but is a recognized consequence of low tidal volume ventilatory strategies. Hypercapnia is usually considered less harmful than larger tidal volumes; thus, a higher Paco2 is “permitted” to allow a lung-protective ventilation strategy (“permissive hypercapnia”). Permissive hypercapnia, first described by Darioli and colleagues [38] in mechanically ventilated patients who had status asthmaticus, involves tolerated increases in Pa

Barriers to implementation

Although the bulk of evidence supports lung-protective strategies in ALI/ARDS with use of low tidal volume ventilation and at least modest levels of PEEP, obstacles to universal adoption across clinical practices still exist [66], [67], [68]. Perceptions surrounding the need for more sedation, the potential for auto-PEEP, and the deleterious effects of hypercapnia loom as potential barriers to implementation of a low tidal volume approach. As described previously, however, current evidence

Recommendations

The authors recommend the following approach to setting the ventilator for patients who have ALI/ARDS:

  • 1.

    Target a tidal volume of 6 mL/kg PBW with a goal of plateau pressures of 30 cm H2O or lower and adjust tidal volume according to ARDSNet guidelines (Box 2). For patients who develop ALI while receiving tidal volumes in excess of 6 mL/kg, stepwise reductions tidal volume of 1 mL/kg every 15 minutes with concomitant increases in respiratory rate to maintain constant minute ventilation is advised

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      Of the estimated 240,000 patients mechanically ventilated in US EDs each year, one-quarter are ventilated for more than 5 h [19,20]. These initial hours of care are influential in the outcome of critically ill patients, as VALI has been shown to occur within minutes to hours of initiating mechanical ventilation [21-23] and progression to ARDS occurs early during ventilation of at-risk patients [7]. For these reasons, initial ventilator settings provided in the immediate post-intubation period can be critically important in determining patient outcomes.

    • Initial mechanical ventilator settings and lung protective ventilation in the ED

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      Based on initial ED ventilator settings, patients in our cohort overall had good respiratory system compliance, with a mean plateau pressure of only 18 cm H2O, well below the goal plateau pressure of 30 cm H2O for lung protective ventilation [6]. Although lung injury has been demonstrated to begin within minutes to hours [3–5], with the low pressures seen in these patients, non–lung protective ventilation may not have caused significant injury. Notably, even patients ventilated with non–lung protective ventilation in our study did not have tidal volumes as large as the control group in the original ARDSNet study, with only 9.6 mL/kg as compared to 12 mL/kg [6].

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      Mechanical ventilation with conventional VTs was associated with a sustained increase in plasma IL-6 levels in one study [27]. Plateau pressures may not accurately reflect the alveolar distension pressure because a multitude of extrapulmonary factors can affect the plateau pressures [28]. The use of esophageal pressure as surrogate for pleural pressure is also problematic [29].

    • A 5-year observational study of lung-protective ventilation in the operating room: A single-center experience

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      Positive end-expiratory pressure (PEEP) is also lung protective because it maintains alveolar recruitment, thus avoiding injury caused by cyclical alveolar opening and closing, as well as the high distending pressure that occurs at the junction of open and collapsed alveoli. Despite controversy about the best level of PEEP, it is generally accepted that a PEEP of 0 cm H2O is harmful in patients with ARDS [2]. In mechanically ventilated patients in the intensive care unit (ICU), it has been shown that adoption of a strategy of limited VT in all patients (< 10 mL/kg IBW) resulted in a lower incidence of ARDS and higher survival [3].

    • Current Knowledge of Acute Lung Injury and Acute Respiratory Distress Syndrome

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