Javier Mauricio Giraldo Sanchez, Diana Lorena Giraldo Arboleda and Ricardo Andres Giraldo Arboleda
During pulmonary embolism, the physiology of the ventilation and the perfusion is damaged. A sudden massive increase of the intrapulmonary shunt might result if the clinical setting is not adequately implemented to regulate the inflammatory process. For this reason, the protection of the ventilation and the tracheal gas insufflation are useful tools in modulating the injury, and the hypercoagulability caused by protein C and S and the deficiency of antithrombin lll. All caused by the damage of the endothelial barrier, therefore gives origin to interstitial leakage, tissue damage, inflammation, and apoptosis.
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