![]() The use of lower VT has also been investigated in the operating room, where randomized trials have associated lower intraoperative VT with reduced occurrence of postoperative pulmonary complications, including ARDS. Beyond reduction in pulmonary complications, this data evaluation suggested greater numbers of ICU-free and hospital-free days as well as reduced all-cause mortality risk. Further, a dose-response relationship between VT size and development of pulmonary complications was suggested ( 4- 6). ![]() Large meta-analytic studies and individual patient analyses of mechanically ventilated ICU patients without ARDS provided evidence for a protective effect of low VT with respect to development of ARDS and/or pneumonia. Nonetheless, subsequent data analyses supported the benefit of using lower VT in patients without a diagnosis of ARDS ( 7). However, the implications of these findings that implied prophylaxis were limited by small study size and early termination of data collection, possibly leading to overestimation of benefit associated with using low VT. ‘Low tidal volume ventilation’, often paired with adjustments of PEEP and frequency, has been labelled as ‘lung protective’ and extended to become a standard in the management of patients with various forms of hypoxemic respiratory failure, and even to those without lung disease or dysfunction ( 4, 5).įollowing the seminal ARMA trial of low VT in ARDS, another randomized controlled trial reported reduced development of ARDS in intensive care unit (ICU) patients allocated to low VT ventilation ( 1, 6). Taken together, such observations have encouraged important revision of the ventilation support paradigm. Reported benefit from lower VT apparently extends to patients making spontaneous breathing efforts as well. However, this latter contention is still hotly debated. In fact, it has been reported that using lower VT confers benefit even when the plateau and driving pressures are relatively low. Nonetheless, the bulk of clinical data now available do support the use of lower VT and de-emphasize prioritizing normal PaCO 2 and pH. It should be noted, however, that this presumed causal link between ventilator settings and outcome has never been proven. The National Institutes of Health (NIH)-sponsored ARDSNet study that compared 6 to 12 mL/kg of PBW (ARMA trial) convincingly demonstrated that the use of relatively low VT in patients with diverse forms and severities of Acute Lung Injury and Acute Respiratory Distress Syndrome (ARDS) may reduce mortality, presumably by reducing injurious lung stretch and systemic release of inflammatory mediators or toxins ( 1). Lung damage secondary to large VT has also been linked experimentally to injury of remote organs ( 1- 3). Animal studies that employ large VT associated with high airway pressures reveal regional disruption of the blood-gas interface, together with inflammation, atelectasis, and hypoxemia, especially in pre-injured lungs. ![]() Elevated airway pressures potentially incur damaging stretch in those lung units that remain aerated. A frequent consequence of using larger VT was the application of abnormally high airway pressures and alveolar forces, especially in patients with acute lung injury, a condition in which the functioning lung is small and both lung collapse and edema are prevalent. While these volumes had long been noted to exceed those of healthy subjects, they were considered necessary for intubated and mechanically ventilated patients to prevent progressive atelectasis, avoid dyspnea and maintain appropriate ventilation. ![]() Prior to publication of the ARDSNet trial of tidal volumes (VT) ( 1), traditional mechanical ventilation often employed VT of 10–15 mL/kg of unadjusted body weight. ![]()
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