We hypothesized that lung-protective mechanical ventilation with lower tidal volumes, as compared to conventional mechanical ventilation induces less inflammation in critically ill patients without evidence of lung disease. Thus, it is not known whether short-term mechanical ventilation with PEEP and moderate to high V T could induce signs of pulmonary or/and a systemic inflammation. However, most studies used high V T and no PEEP in comparison to low V T and PEEP. Three randomized studies on surgical patients suggested that a pulmonary inflammatory response could be induced by a short-term mechanical ventilation (up to 10 hours) even in lungs without pre-existing injury. Retrospective observations suggest that higher V Ts may be deleterious after prolonged ventilation or major surgery. Observational studies have showed that a lung inflammatory response could be induced after conventional and prolonged mechanical ventilation in a mixed population of critically ill patients. In contrast to patients with acute lung injury having a continuing systemic inflammatory reaction, it is not clear if MV by itself can initiate lung inflammation. The clinical repercussion of these studies is uncertain because unphysiologically large V Ts and no PEEP were generally compared to low V T and PEEP. Experimental data suggest that mechanical ventilation with higher V T and zero end-expiratory pressure (ZEEP) induces not only cytokine release but also translocation of cytokines from the lungs to the systemic circulation and even vice versa. In contrast, mechanical ventilation with moderate-to-high levels of PEEP and low V T of approximately 6 mL/kg predicted body weight assured adequate gas exchange, decreased intraalveolar and systemic mediator levels, and improved outcome. In such patients, with existing pulmonary and systemic inflammation, ventilation with tidal volumes (V T) of 10 to 15 mL/kg predicted body weight and low-to-moderate levels of positive end expiratory pressure (PEEP) was associated with increased intraalveolar and systemic levels of inflammatory mediators. Trial RegistrationĬlinical studies suggest that mechanical ventilation (MV) can modify inflammatory responses in patients with acute lung injury. The use of lower tidal volumes may limit pulmonary inflammation in mechanically ventilated patients even without lung injury. After 12 hours, BALF TNF-α ( P = 0.03) and BALF IL-8 concentrations ( P = 0.03) were higher in the high V T group than in the low V T group. While initial analysis did not reveal significant differences, standardization against urea of logarithmic transformed data revealed that TNF-α and IL-8 levels in bronchoalveolar lavage (BAL) fluid were stable in the low V T group but increased in the high V T group ( P = 0.04 and P = 0.03). At admission or after 12 hours there were no differences in serum TNF-α and IL-8 between the two groups. Twenty patients were enrolled and analyzed. TNF-α and IL-8 concentrations were measured in the serum and in the bronchoalveolar lavage fluid (BALF) at admission and after 12 hours of study observation time. Patients were randomized to receive MV either with tidal volume (V T) of 10 to 12 ml/kg predicted body weight (high V T group) (n = 10) or with V T of 5 to 7 ml/kg predicted body weight (low V T group) (n = 10) with an oxygen inspiratory fraction (FIO 2) enough to keep arterial oxygen saturation >90% with positive end-expiratory pressure (PEEP) of 5 cmH 2O during 12 hours after admission to the study. Patients without lung disease and submitted to mechanical ventilation admitted to one trauma and one general adult intensive care unit of two different university hospitals were enrolled in a prospective randomized-control study. We compared the effects of a protective versus a conventional ventilatory strategy, on systemic and lung production of tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) in patients without lung disease. Mechanical ventilation (MV) with high tidal volumes may induce or aggravate lung injury in critical ill patients.
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