Abstract
Hypoxia is a hallmark of acute respiratory distress syndrome (ARDS) [1] and a major therapeutic goal is to improve arterial oxygen content. The mechanism underlying hypoxia is true intrapulmonary shunt [2] due to non-ventilated, perfused alveoli with little contribution of ventilation-perfusion mismatching. The increase in inspiratory oxygen concentration is not enough to correct hypoxia (refractory hypoxia), and reopening closed lung units represents the only way to improve gas exchange. Three principal reasons account for alveolar exclusion from ventilation:
-
1)
the filling of the air spaces by exudate, pseudomembranes, cellular debris and inflammatory cells as consequence of the structural damage of the alveolo-capillary unit;
-
2)
the collapse of small airways as a consequence of reduced lung volume and loss of the lining surfactant [3]; and
-
3)
atelectasis due to compression of dependent lung units by increased weight of the overlying edematous lung parenchyma [4] or high O2 concentrations [5].
Keywords
- Inflection Point
- Acute Respiratory Distress Syndrome
- Acute Respiratory Failure
- Respir Crit
- Functional Residual Capacity
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Mergoni, M., Volpi, A., Rossi, A. (1997). Inflection Point and Alveolar Recruitment in ARDS. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1997. Yearbook of Intensive Care and Emergency Medicine, vol 1997. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-13450-4_46
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