Hemodynamique et echanges gazeux dans l'embolie pulmonaire: physiopathologie et traitement. [Hemodynamics and gas exchange in pulmonary embolism: physiopathology and treatment]

Détails

ID Serval
serval:BIB_8A193CA36F23
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Hemodynamique et echanges gazeux dans l'embolie pulmonaire: physiopathologie et traitement. [Hemodynamics and gas exchange in pulmonary embolism: physiopathology and treatment]
Périodique
Schweizerische Medizinische Wochenschrift
Auteur(s)
Feihl  F.
ISSN
0036-7672 (Print)
Statut éditorial
Publié
Date de publication
11/1991
Volume
121
Numéro
45
Pages
1645-53
Notes
English Abstract
Journal Article
Review --- Old month value: Nov 9
Résumé
Pulmonary emboli can cause severe hemodynamic and respiratory disorders whose physiopathologic mechanisms need to be well understood to ensure appropriate treatment. In previously healthy subjects only massive obstructions (greater than 50%) have dangerous effects due to the very large functional reserve of the pulmonary vascular bed. The same is not always true where there are previous anomalies of pulmonary circulation. In man, vascular obstruction appears to be primarily mechanical, although the presence of emboli may also trigger the release of vasoconstrictor mediators. In the animal it is accepted that these mediators may play an important role, in particular by increasing the critical closing pressure in pulmonary microcirculation. Apart from resistance to continuous bloodflow, the vascular obstruction may accentuate a number of dynamic phenomena specifically obstructing the passage of a pulsatile flow. The aggregate obstacles to right ventricular ejection are known by the term pulmonary artery impedance. Gas exchanges can be disturbed by a wide variety of mechanisms. Arterial hypoxemia chiefly results from maldistribution of the ventilation/perfusion ratio and, in severe forms associated with a fall in cardiac output, from diminution of the partial oxygen pressure of mixed venous blood. The right auricular pressure increase may sometimes contribute to hypoxemia by causing reopening of a permeable ductus Botalli with onset of right-left shunt. This possibility should be considered if oxygen administration does not correct hypoxemia. The dead space effect is not always in relation to the size of the vascular obstruction due to hypocapnic bronchoconstriction in the hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS)
Mots-clé
Anoxemia/physiopathology Cardiac Output Cardiac Output, Low/therapy *Hemodynamic Processes Humans Pulmonary Diffusing Capacity Pulmonary Embolism/*physiopathology/therapy *Pulmonary Gas Exchange Pulmonary Wedge Pressure Respiratory Dead Space Vasoconstriction Ventilation-Perfusion Ratio Ventricular Function, Left
Pubmed
Web of science
Création de la notice
25/01/2008 10:38
Dernière modification de la notice
03/03/2018 19:09
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