Respiration Assist By Pumpless Extracorporeal Oxygenation To ARDS Induced By Inhalation Of Perfluoroisobutylene

Perfluoroisobutelene(PFIB) is a kind of low-molecular-weight fluorocarbon compound, which exists as colorless gas with almost no smell at normal tempetature. PFIB is of the same kind of toxic gas as phosgene, but ten times as toxic as phosgene, and inhalation of PFIB can induce severe lung injury . PFIB can be generated as a commom byproduct in fluoropolymer industry, and also by pyrolysis of Teflon with temperature above 300 C . As Teflon is of many benifitial properties, it is widely used in people life, so poisoning cases by inhalation of PFIB often happen during fire accidents .Up to now, the specific mechamisms of PFIB' s toxic funtion has not been thoroughly interpreted, correspondingly we can take little anti-measures to protect and treat. From view of clinical medicine, we for the 1st time chose big animal(mongrel) as poisoned object, several work has been finished as follows:1. Constructed inhalation system fit for mongrel to ensure that concentration of PFIB during inhalation by mongrel kept stable and constant (p>0.05)o We established that PaO2/FiO2 of mongrel invariably reached level ofARDS 22 hours after inhalation of PFIB with concentration of 0.30-0.32mg/L for 30 minutes, and by observation of clinical signs and pathologicchanges we concluded that inhalation of PFIB induced severe ARDS.2. We measured levels of TNF-a, IL-6, IL-8 in mongrel blood circulation before and after inhalation of PFIB, and found level of IL-8 elevated significantly after inhalation, whereas the other two cytokines did not change significantly. Thereby we speculated that lung injury after inhalation of PFIB may be result of PMN recruitment and activation in lung during latency.3. We studied therapeutic effect of artery-vein pumpless ECMO: as control, assist by ventilator is capable of increase mongrel' s SaO2, but as the lung gradually became solid, basic oxygen intake of mongrel could hardly be provided by ventilator; as for ECMO group, we began ventilator assist on ARDS model first. As soon as it can not keep SaO2 above 90%, we start A-V pumpless ECMO using jugular vessels,, As lung area capable of air exchange reduced significantly and area of the oxygenator used is also limited, the ECMO is not capable of complete oxygenation by itself . When combined with mechanical ventilation, SaO2 kept above 90%, and PaCO2 kept between 20 and 30mmHg. Moreover A-V pumpless ECMO is capable of reducing model ' s PAP ( p<0.05 ) , thereby improve right ventricular function. After 40 hours ECMO were ended, and pathologic examination of lung show signs of improvement.