![]() 15 Of note, as was the case with the ARDSNet study, the initial static respiratory system compliance was better in the group that went on to develop ARDS (higher V T group). The initial ventilator settings, in particular the V T, were associated with the development of ARDS. 14 The same group then followed up with an analysis of a large international mechanical ventilation database of subjects who received mechanical ventilation for >48 h but did not have ARDS at the outset. Figure 1 illustrates that, as V T increased, the ALI rate also increased. 14 They concluded that there existed 2 important risk factors for the development of ALI: large V T values and the administration of blood products. They found that 80 subjects (24%) developed ALI within the first 5 d and, on average, within the first 3 d. Shortly after the ARDS Net study in 2000, Gajic et al 14 conducted a retrospective cohort study of 332 medical-surgical subjects receiving mechanical ventilation for >48 h who did not have acute lung injury (ALI) at the onset of mechanical ventilation. 13 What we do not know for sure is whether higher V T values have this on effect on normal lungs. 2, 12 The biophysical injury in ARDS lungs consists of overdistention of recruited alveoli, direct cell damage due to cyclical opening and closing of unstable alveoli, and loss of surfactant function. ![]() The use of high V T values in patients with ARDS clearly appears to be detrimental in that it rapidly results in pulmonary changes that mimic and amplify the ARDS inflammatory process. Ventilation of Patients Who Do Not Have ARDSĪlthough mechanical ventilation strategies are slowly gravitating toward the use of lung-protective ventilation, many clinicians have not adopted the practice in all patients. 12 Since the publication of this study, there has been a growing body of evidence that suggests that the use of lower V T values may also improve clinical outcomes in patients without ARDS. The study was stopped early after an interim analysis revealed a survival advantage of 22% in the lower V T group. ![]() It was a large multi-center prospective randomized trial with >800 subjects enrolled. However, in 2000, a landmark study comparing lower V T values (6 mL/kg PBW) with higher V T values (12 mL/kg PBW) in ARDS was undertaken by the ARDS Net group. 9– 11 These studies were hampered by several factors, including higher than predicted mortality in the control group, a relatively small difference in V T between the groups, insufficient statistical difference to detect a signal, and uncorrected acidosis in the low V T group. Several small human studies were reported in the mid- to late 1990s that produced conflicting results. 2– 8 With the emergence of these animal data, clinicians began to question the traditional use of V T values in the range of 10–15 mL/kg PBW in humans. Animal studies have shown that high V T ventilation increases levels of pro-inflammatory mediators, leads to pulmonary edema, and causes increased alveolar-capillary permeability and structural abnormalities. There is a plethora of preclinical evidence from animal studies supporting the fact that the use of high V T values can directly cause injury to normal lungs. This will be done with viewpoints from both the pro and con positions. The aim of this paper is to examine the evidence relating to the use of lower V T values in conditions other than ARDS in which mechanical ventilation is required. ![]() 1 There is a growing body of evidence that points toward the use of lower V T values leading to improved outcomes in patients suffering from other forms and degrees of respiratory failure. Since we now know that the use of lower V T strategies (more specifically 6 mL/kg PBW) helps to limit the pulmonary damage during ARDS, the question now is: Should we be using this strategy in all mechanically ventilated patients? Anatomically speaking, it makes sense to, since the normal physiologic V T for humans is approximately 6 mL/kg PBW. The use of lower tidal volume (V T) values, 4–8 mL/kg predicted body weight (PBW) is part of this lung-protective strategy for mechanical ventilation (mechanical ventilation) along with limiting the plateau pressure to a maximum of 30 cm H 2O and prudent use of PEEP to prevent atelectasis. Lung-protective ventilation has evolved over the past couple of decades to the point that it has become standard of care for patients with ARDS. It is well known that the use of mechanical ventilation has the potential to aggravate pulmonary injury, but emerging evidence indicates that it may also precipitate lung injury in patients with no previous injury. ![]()
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