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Pharmacologic Approach of Hypoxemia in ARDS Patients

  • Conference paper
Yearbook of Intensive Care and Emergency Medicine

Part of the book series: Yearbook of Intensive Care and Emergency Medicine ((YEARBOOK,volume 1996))

Abstract

Acute pulmonary hypertension is frequently observed in patients with acute respiratory distress syndrome (ARDS) and is caused by vasoconstriction and anatomical remodeling of pulmonary vessels [1]. Vasoconstriction of pulmonary vessels appears related to hypoxic pulmonary vasoconstriction, circulating mediators like thromboxane A2 and endothelial-released vasoconstrictors like platelet activating factor (PAF) and endothelin. Constriction of pulmonary vessels is likely non-homogeneously distributed because the pulmonary endothelium may also release vasodilator substances like prostacyclin and nitric oxide (NO) which counteract pulmonary vasoconstriction. The lack of constriction in the non-ventilated parts of the lung results in an increased local blood flow which tends to increase pulmonary shunt leading to life-threatening hypoxemia. Anatomical remodeling of pulmonary vessels is made of muscular hypertrophy, microthrombosis, fibrosis and destruction of pulmonary vessels [2, 3]. The pulmonary vasoconstriction can be reversed by vasodilators whereas pulmonary vasodilation will be reversed by vasoconstrictors.

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Authors
  1. L. Puybasset
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  2. J. J. Rouby
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Editors and Affiliations

  1. Department of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, B-1070, Brussels, Belgium

    Jean-Louis Vincent (Clinical Director) (Clinical Director)

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© 1996 Springer-Verlag Berlin Heidelberg

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Puybasset, L., Rouby, J.J. (1996). Pharmacologic Approach of Hypoxemia in ARDS Patients. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 1996. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80053-5_38

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  • DOI: https://doi.org/10.1007/978-3-642-80053-5_38

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