THE OUTLOOK FOR MECHANICAL VENTILATION IN ARDS

Citation
M. Max et al., THE OUTLOOK FOR MECHANICAL VENTILATION IN ARDS, Schweizerische medizinische Wochenschrift, 127(24), 1997, pp. 1030-1038
Citations number
68
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00367672
Volume
127
Issue
24
Year of publication
1997
Pages
1030 - 1038
Database
ISI
SICI code
0036-7672(1997)127:24<1030:TOFMVI>2.0.ZU;2-T
Abstract
Despite more than 25 years of extensive research, the mortality of ARD S patients remains high. The inflammatory process within the lung and the associated gas exchange disturbances require an aggressive ventila tory regimen, which itself may harm the lung. Therapeutic measures whi ch are used to reduce iatrogenic damage to the lung are pressure contr olled mechanical ventilation in combination with PEEP and permissive h ypercapnia, dehydration and extracorporeal gas exchange. At present, n ew strategies such as intratracheal instillation of surfactant, partia l liquid ventilation and inhalation of nitric oxide (NO) are being eva luated. Surfactant reduces the surface tension, forming a monomolecula r layer at the air/tissue interface. It thereby decreases the forces n ecessary to expand the alveoli and prevents alveoli with small diamete r from collapsing. In ARDS, a disturbance of surfactant synthesis, fun ction and re-uptake is the rationale for treatment with exogenous surf actant. Initial clinical results suggest a limited positive effect ind ependently of the surfactant preparation used, the dose and the applic ation mode. Experience with partial liquid ventilation with perfluoroc arbons in ARDS has also been reported. Perfluorocarbons are liquids wi th a high binding capacity for oxygen and carbon dioxide. During norma l mechanical ventilation with gas, repetitive doses of perfluorocarbon s are instilled into the lungs up to a volume equal to the functional residual capacity. The liquid is pushed into collapsed alveoli and kee ps them open by reducing the surface tension. First clinical studies h ave demonstrated the possible improvement in pulmonary gas exchange.In ARDS, inhalation of NO may cause a predominantly selective vasodilati on in blood vessels of ventilated lung regions, resulting in an increa se in PaO2 and a decrease in pulmonary artery pressure. The effect of NO on the pulmonary vasculature also induces a reduction in right vent ricular afterload and also in pulmonary capillary pressure, which may lead to a faster resolution of pulmonary edema. However, in spite of t he promising results of these new strategies, further studies are need ed to evaluate their influence on morbidity and mortality.