Does the use of high PEEP levels prevent ventilator-induced lung injury?

Abstract

Overdistention and intratidal alveolar recruitment have been advocated as the main physical mechanisms responsible for ventilator-induced lung injury. Limiting tidal volume has a demonstrated survival benefit in patients with acute respiratory distress syndrome and is recognized as the cornerstone of protective ventilation. In contrast, the use of high positive end-expiratory pressure levels in clinical trials has yielded conflicting results and remains controversial. In the present review, we will discuss the benefits and limitations of the open lung approach and will discuss some recent experimental and clinical trials on the use of high versus low/moderate positive end-expiratory pressure levels. We will also distinguish dynamic (tidal volume) from static strain (positive end-expiratory pressure and mean airway pressure) and will discuss their roles in inducing ventilator-induced lung injury. High positive end-expiratory pressure strategies clearly decrease refractory hypoxemia in patients with acute respiratory distress syndrome, but they also increase static strain, which in turn may harm patients, especially those with lower levels of lung recruitability. In patients with severe respiratory failure, titrating positive end-expiratory pressure against the severity of hypoxemia, or providing it in a decremental fashion after a recruitment maneuver, is recommended. If high plateau, driving or mean airway pressures are observed, prone positioning or ultraprotective ventilation may be indicated to improve oxygenation without additional stress and strain in the lung.

Figure 1

Mean airway pressures in Oscillate (squares) and Oscar (circles) studies. Data are from tables 3S and 4S (Oscillate) and from table 2 (Oscar). In the Oscar trial, mean airway pressures in the control arm were not given and were calculated as P_mean=PEEP + 1/3(Δ P_plateau-PEEP), considering an inspiratory time from 1:2. HFOV - high-frequency oscillatory ventilation.

Figure 2

Effect of increasing levels of positive end-expiratory pressure on alveolar recruitment, tidal recruitment and derecruitment and static strain. From zero end-expiratory pressure to a positive end-expiratory pressure of 5cmH₂O, there was marked recruitment and a decrease in recruitment and derecruitment, which provided a protective effect. Positive end-expiratory pressure levels above 15cmH₂O should be carefully titrated, as the impact on recruitment is less evident and strain may increase.

Figure 3

Effect of different tidal volumes on tidal recruitment and derecruitment, partial pressure of carbon dioxide levels and transpulmonary pressure. A decrease in tidal volume will always induce a decrease in transpulmonary pressure, but a very low tidal volume may increase partial pressure of carbon dioxide and decrease pH. Vt - tidal volume; R/D - tidal recruitment and derecruitment; PaCO₂ - partial pressure of carbon dioxide; P_L - transpulmonary pressure.