• N Burk, J L Benumof, G T Ozaki, L Miller, and H B Howell.
• Department of Anesthesia, University of California, San Diego School of Medicine, La Jolla 92093.
• J. Cardiothorac. Vasc. Anesth. 1991 Feb 1;5(1):46-50.

AbstractIt has been previously reported that continuous insufflation of low-flow O2 (0.05 to 0.20 L/kg/min), both supracarinally and subcarinally, in addition to intermittent positive-pressure ventilation (IPPV) (IPPV + O2 at a specific flow rate) caused progressive hemodynamic deterioration in patients. As demonstrated in a subsequent mechanical lung model, the hemodynamic deterioration was most probably due to lung hyperexpansion. The purpose of this study was to test the hypothesis that the O2 retarded the outflow of gas from the lung during exhalation and that if the insufflation were limited to the period of time from the end of tidal exhalation (EE) to the beginning of the next IPPV tidal inspiration (BI), lung hyperexpansion would not occur. The use of intermittent O2 in addition to IPPV was studied in both a mechanical lung model and in patients under general anesthesia; the mechanical lung model permitted direct examination of lung volume, and the patient study allowed determination of gas exchange effects. In the mechanical lung model and in the patients, a wide range of EE-BI O2 flow rates were used; respectively, 1 to 40 L/min and 0.05 to 0.20 L/kg/min. In the mechanical lung model, lung pressure and volume at EE and end-inspiration did not increase as long as the O2 flow was kept at or below 10 L/min. In the patients, airway pressure and hemodynamics did not change appreciably, but there was also no increase in CO2 elimination.(ABSTRACT TRUNCATED AT 250 WORDS)

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