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Atelectasis during uneven mechanical ventilation leads to alveolar hypoxia and could therefore result in lung inflammation and injury.
Mechanical ventilation leads to inappropriate deposition and elastin breakdown accompanied by distortion of further septation [17 19].
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].
Such findings demonstrated that high-volume mechanical ventilation leads to pulmonary edema of the permeability type.
Inactivity of the diaphragmatic muscles during mechanical ventilation leads to atrophy and contractile dysfunction.
A 'second hit', or subsequent insult, such as mechanical ventilation, leads to an overwhelming pulmonary inflammatory response.
Similar(53)
Our data support the notion that both too low and too high volumes in mechanical ventilation lead to lung damage.
In ALIp, mechanical ventilation led to myofibril damage with Z-disk edema, which was greater under PCV and BIVENT-100 than with other ventilator strategies.
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.
High tidal volume mechanical ventilation (HTVMV) leads to pulmonary edema from increased endothelial permeability.
Related(20)
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