Citation

Petit P. Ann. Anesthesiol. Fr. 1980; 21(6): 695-698.

Vernacular Title

Oedemes pulmonaires d'origine toxique. Donnees hemodynamiques.

Copyright

(Copyright © 1980, Association Des Anesthesiologistes Francaise)

DOI

unavailable

PMID

6111279

Abstract

The inhalation of toxic gases or vapours is capable of resulting in pulmonary oedema (P.O.), the mechanism of which corresponds, on the basis of a number of hemodynamic studies carried out, to that which characterises the so-called "lesional" pulmonary oedema, which is different from so-called "hemodynamic" oedema. Classically PAP, PCP and P wedge pressure have virtually normal values (normalisation of pulmonary arterial hypertension by correction of hypoxemia). CI and SWILV are normal or increased and pulmonary resistances are virtually normal. The origin of the oedema is thus related to an increase in alveolo-capillary permeability. The inhalation of toxic gases or vapours with a caustic or irritant action, or containing particles, however, usually adds on an obstructive syndrome, similar to a severe asthmatic attack. Under such conditions, the marked reduction in intrathoracic pressure during inspiration definitely favours pulmonary oedema by decreasing intra-alveolar pressure and by the accumulation of blood in the pulmonary circulation, and is capable of masking pulmonary arterial hypertension. Raised pressure, related to expiratory effort, on the contrary, decreases venous return and may result in collapse of the capillaries. Whilst the principal mechanism of PO by the inhalation of toxic gases or vapours is related to an increase in alveolo-capillary permeability, it is nevertheless important not to under-estimate the role of variations in intra-thoracic pressures which may constitute a provoking or at least aggravating element.

Language: fr