par Leeman, Marc 
;Naeije, Robert
Référence Réanimation, 13, 2, page (131-135)
Publication Publié, 2004
;Naeije, Robert Référence Réanimation, 13, 2, page (131-135)
Publication Publié, 2004
Article révisé par les pairs
| Résumé : | Pulmonary artery pressure increases in almost all patients with the acute respiratory distress syndrome. The elevation is attenuated by the release of endogenous vasodilators which counterbalance the effects of endogenous vasoconstrictors. By inhibiting hypoxic pulmonary vasoconstriction, the endogenous vasodilators contribute to the increase in intrapulmonary shunt. On the other hand, the administration of vasodilators in the airways, such as nitric oxide, reduces pulmonary artery pressure and improves gas exchange by diverting pulmonary blood flow to better-ventilated regions. These beneficial effects have unfortunately not been associated with an increased survival in patients with the acute respiratory distress syndrome. The rise in pulmonary artery pressure increases right ventricular afterload and can lead to acute cor pulmonale. The frequency and mortality of this complication have recently decreased, perhaps in relation with the use of lower tidal volumes during mechanical ventilation, which limit the plateau pressure, the compression of pulmonary vessels by the airways, and the right ventricular afterload. © 2003 Société de réanimation de langue française. Publié par Elsevier SAS. Tous droits réservés. |
