Mechanical ventilation leads to inappropriate deposition and elastin breakdown accompanied by distortion of further septation [17 19].
Atelectasis during uneven mechanical ventilation leads to alveolar hypoxia and could therefore result in lung inflammation and injury.
The pathogenesis of ARDS can start when loss of surfactant function, caused by ventilation (either spontaneous or mechanical ventilation), leads to collapsed alveoli that act as SC in the tissue surrounding them [52, 53].
A 'second hit', or subsequent insult, such as mechanical ventilation, leads to an overwhelming pulmonary inflammatory response.
The use of a high-protein diabetes-specific EN formula in hyperglycemic critically ill patients on mechanical ventilation leads to lower insulin requirements, reduces plasma and capillary blood glucose levels and glycemic variability, and could also reduce the risks of ICU-acquired ventilator-associated pneumonia and tracheobronchitis when compared with that of a standard high-protein formula.
Our data support the notion that both too low and too high volumes in mechanical ventilation lead to lung damage.
Complications and the need for prolonged mechanical ventilation lead to an increase in diagnostic procedures, invasive monitoring and the amount of drugs and blood products, and thus lead to an increase of the daily cost per patient [ 2, 3, 5- 10].
A second-hit model theory can be suggested as a mechanism by which mechanical ventilation may lead to ALI/ARDS.
Introduction: Although necessary, mechanical ventilation can lead to ventilator-induced lung injury (VILI) even when using protective ventilation strategies that combine low tidal volume (Vt)(6 ml kg predicted body weight) and plateau pressure (Pplat) <= 30cmH20.
However, mechanical ventilation can lead to lung injury by different mechanisms, with subsequent diffuse alveolar damage, pulmonary edema, and local production of inflammatory mediators.
