ABSTRACT
The acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that
may occur in any patient without any predisposition and that is mostly triggered by
underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and
pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest
x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia
with a PaO2 /FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%[1 2 3 2 /FiO2 values between 200 and 300mmHg. Despite ongoing and intensive scientific research
in this area, the mechanisms underlying ALI/ARDS are still not completely understood,
and until recently, there were no studies demonstrating any beneficial effect of a
single treatment modality in ARDS. The recent report that a specific approach to ventilatory
support can significantly reduce mortality in ARDS underscores the need for better
understanding of the pathophysiological events occurring in this syndrome. This review
therefore summarizes the current pathophysiological concepts underlying the evolution
of acute hypoxemic respiratory failure and focuses on: (1) possible reasons for the
development of ALI/ARDS; (2) cellular and humoral mediator responses leading to a
sustained and self-perpetuating inflammation of the lung; (3) consequences with regard
to fluid balance, pulmonary perfusion, ventilation, and efficiency of gas exchange;
and (4) mechanisms underlying the aggravating complications commonly seen in ARDS,
especially ventilator-associated lung injury, ventilator-associated pneumonia, and
lung fibrosis.
KEYWORD
Surfactant - pathophysiology of ARDS - cytokines - fibrosis - coagulation
