The oxygen need not get into the blood stream to cause damage and result in atelectasis. The article cited below by Dr. Marini provides insight into recent thinking about the relationship between high pressures and lung damage. It also mentions inspired oxygen concentration as another factor. Absorption is not the only cause of atelectasis. Alterations in surfactant caused by high oxygen concentrations, is another. It remains important to monitor continuously and titrate the inspired oxygen fraction to the lowest level that, in conjunction with PEEP, will result in an acceptable blood oxygen concentration.
American Journal of Respiratory and Critical Care Medicine, Volume 163, Number 4, March 2001, 806-807
Ventilator-induced Airway Dysfunction?
John J. Marini
University of Minnesota, St. Paul, Minnesota
This is a great article to read. Thanks to NJC RN. Also of interest is an article in the same journal, Volume 161 pgs 141-146. This article, done by John G. Laffey and colleagues, discusses in detail the supporting role of permissive hypercapnia when treating patients with ARDS. Well worth reading, MISS MEL..both articles. Take care and good luck.
J.C.I. RRT RCP
ARDS (Acute Respiratory Distress Syndrome) and high FiO2 requirements go hand in hand as you well know. ARDS is typically defined as "...an acute condition characterized by bilateral pulmonary infiltrates and hypoxemia in the absence of cardiogenic origin." A PAO2/FiO2 ratio less than 200 is also indicative of ALI (Acute Lung Injury). If a Swan-Ganz is placed, which it should be if ARDS is suspected, wedge pressures less than 18 or reflective normal left atrial pressures rule out cardiac involvement.
As for your question about the O2 toxicity and the alveolar-capillary membrane as it relates to high FiO2's and absorption atelectasis. In the early stages of ARDS, the A-C membrane permeability is increased allowing for protein-rich fluid to enter into the alveoli, destryoing alveolar cells and actually creating pulmonary edema. The A-C membrane is damged secondary to this fluid from either vascular endothelium damage(sepsis) or alveolar epithelium damage(aspiration/trauma). Damage to these alveolar cells can decrease the surfactant production allowing for alveolar collapse, which results in poor O2 exchange. As stated before, high FiO2's are required during ARDS. However, it is indicated that it is still important to lower FiO2 levels to appropriate levels (<65%) to maintain SaO2's between 85-90% to minimize absorption atelectasis and worsening ALI. This can be done with the addition of PEEP and Pressure Controlled Ventilation (PCV) with Inverse I:E Ventilation Ratios (2:1). Also, numerous medical centers, including one I am affiliated with, have had success with prone ventilation trials. Your question is rational but it is not right thinking to ignore FiO2 levels in ARDS. Adding PEEP and utilizing alternative modes of ventilation can greatly improve O2 status while lowering the FiO2. Studies are also showing allowing permissive hypercapnia(increased CO2 levels) so to minimize increased airway pressures when ventilating non-compliant lungs with increased PEEP levels. It is not uncommon for patients with ARDS who require high PEEP levels to eventually obtain a chest tube(or more than one!) because of barotrauma resultant to increased PEEP. Instead of using the 10-12ml/kg to calculate Vt, using 6ml/kg and allowing slighly increased PCO2 levels minimizes the effect of volutrauma(increased volumes resulting in pneumothroaces). I hope this helps answer your question. Take care...
J.C.I. RRT RCP