Abstract
The major function of the lung is to exchange physiological (respiratory) gases, namely, oxygen (O2) and carbon dioxide (CO2). In normal conditions, an equilibrium between oxygen uptake (VO2) and carbon dioxide elimination (VCO2) in the lungs, and the metabolic demands regarding oxygen consumption and carbon dioxide production, must be attained with whatever partial pressures of both gases in arterial blood are necessary to achieve this equilibrium. Only when the lungs fail as a gas exchanger do arterial hypoxemia and hypercapnia or both appear, and respiratory failure ensues. Arterial oxygen (PaO2) and carbon dioxide (PaCO2) tensions are the directly measurable end-point variables used routinely by clinicians to properly manage patients with acute respiratory failure. When this is severe, mechanical ventilation is then considered the best strategy for treating patients. Traditionally, the mechanisms of hypoxemia are alveolar hypoventilation, limitation of alveolar to end-capillary O2 diffusion, shunt, and ventilation-perfusion (VA/Q) mismatching; major causes of hypercapnia are alveolar hypoventilation and VA/Q inequalities [1].
Supported by the Comissionat per a Universitats i Recerca, Generalitat de Catalunya (1999 SGR 00228)
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Ferrer, M., Roca, J., Rodriguez-Roisin, R. (2003). Cardiopulmonary Interactions and Gas Exchange During Weaning from Mechanical Ventilation. In: Mancebo, J., Net, A., Brochard, L. (eds) Mechanical Ventilation and Weaning. Update in Intensive Care Medicine, vol 36. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56112-2_11
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DOI: https://doi.org/10.1007/978-3-642-56112-2_11
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