Tidal volume in patients with normal lungs during general anesthesia: lower the better?

L UNG protective mechanical ventilation strategies using low tidal volumes (VT) of approximately 6 ml/kg predicted body weight and moderate or high positive end-expiatory pressures (PEEP) have been demonstrated to improve relevant outcome measures in patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Despite the fact that lowering VT failed to improve outcomes in three other controlled trials investigating VT in ALI and ARDS patients, there is unequivocal evidence that mechanical ventilation in critically ill patients has the potential to aggravate or, under certain circumstances, initiate lung injury. In addition to mechanical ventilation with lower VT, patients with ALI and ARDS could benefit from strategies that avoid cyclic alveolar collapse and tidal recruitment, including the use of higher levels of PEEP. Meta-analysis suggest this approach can not only waive the need for rescue therapies as a result of life-threatening hypoxemia, it can also reduce mortality in patients with more severe ALI. It is still matter of discussion whether or not lung protective strategies could be beneficial in ventilated patients without ALI or ARDS as well. In this issue of ANESTHESIOLOGY, Sundar et al. studied the use of low VT ventilation on duration of postoperative mechanical ventilation among patients with normal lungs who underwent elective cardiac surgery. Mechanical ventilation is often mandatory for patients who undergo surgery, especially cardiac surgery. Despite its life-saving necessity, mechanical ventilation adds mechanical stress to lung tissues and may cause damage on a cellular level. Potential mechanisms include: (1) stress failure of plasma membrane (necrosis, release of mediators and cytosol from damaged cells), (2) stress failure of endothelial and epithelial barriers (loss of compartmentalization, hemorrhage, accumulation of lung leukocytes), (3) damage of the extracellular matrix, (4) overdistension without tissue destruction, (5) effects on the vasculature independent of stretch and rupture (increased intraluminal pressure and shear stress). In contrast with results from small animal models—in which mechanical stress induced by high VT and low (or no) PEEP has caused lung injury in normal lungs (and which have been recently seen in larger animals in the context of high VT) — effects of short-term perioperative mechanical ventilation on pulmonary integrity in patients are less well defined. Two retrospective analyses identified high airway pressures and VT as independent risk factors for ALI and ARDS in critically ill patients who require mechanical ventilation for reasons other than ALI or ARDS. Studies on mechanical ventilation in perioperative settings often make use of small patient populations and focus at different (and not necessarily clinically relevant) outcomes, such as inflammatory mediators. Such studies have revealed inhomogeneous results. The impression is, however, that major surgery (e.g., cardiac surgery), which per se causes a clinically relevant inflammatory response, makes the lungs more vulnerable to injury caused by mechanical stress. This effect might be explained by a twoor multiplehit model. Accordingly, potentially injurious mechanical ventilation as a second hit requires preexisting injury caused by ALI/ ARDS. Alternatively, it may also be a marked inflammatory response (e.g., triggered by major surgery) to cause or aggravate lung injury and/or systemic inflammation. Different studies on mechanical ventilation strategies during and/or after cardiac surgery are summarized in table 1. The present study by Sundar et al. is the largest one in cardiac surgery patients and it focuses on clinically relevant outcomes. Although the authors failed to show a significant difference in time on mechanical ventilation, the number of patients still on mechanical ventilation at 6 and 8 h after surgery was significantly lower in the protective ventilation group. However, there are several limitations of this study: (1) it is a single-center study, thus its results cannot be generalized to other centers or other groups of patients; (2) obese patients were not included in the study; (3) the level of PEEP was selected according to a specific table and not via individual physiologic parameters like gas-exchange, compliance, or oxygen delivery; and (4) weaning procedures were not specifically standardized. In this study, PEEP levels in both study groups were approximately 5 cm H2O. Low PEEP levels might increase regional shear stress and lung injury by causing opening and closing of lung units within a ventilatory cycle (atelectrauma), even in absence of high plateau pressures. Tidal recruitment and derecruitment can be minimized by using PEEP levels of 10 cm H2O during anesthesia, at least in healthy nonobese patients. 20