Continuous oxygen insufflation in addition to IPPV causes air trapping in a mechanical lung model

It has previously been reported that continuous insufflation of either supracarinal or subcarinal oxygen in addition to intermittent positive-pressure ventilation (IPPV) in patients under general anesthesia, and in critically ill patients in the intensive care unit, causes increased proximal airway pressure, decreased systemic blood pressure, and decreased cardiac output. The investigators hypothesized that these deleterious hemodynamic effects were due to intrapulmonary air trapping, resulting in an increased distal intrapulmonary pressure and volume. The purpose of this study was to test this hypothesis in an appropriate mechanical lung model. The study determined end-inspiratory and end-expiratory lung pressures and volumes during eight experimental sequences: (1) IPPV alone; (2) insufflation of oxygen alone at 2.5, 5.0, and 10.0 L/min (O2-2.5, 5.0, 10.0); (3, 4, and 5) IPPV plus insufflation of oxygen (IPPV + O2-0.0, 2.5, 5.0, 10.0) through a supracarinal catheter (sequence 3), subcarinal catheters (sequence 4), and through a CO2 sampling port of an endotrachael tube (sequence 5); (6 and 7) IPPV + O2-5.0 with increased expiratory time caused by an increased inspiratory flow rate (sequence 6) and a decreased respiratory rate (sequence 7); (8) IPPV + O2-5.0 with increased airway diameter. Experimental sequences 1 and 2 resulted in no increases or minimal ones in lung pressure and volume, respectively. With each insufflation catheter system (sequences 3, 4, and 5), each incremental increase in insufflation flow rate resulted in significant increases in lung pressure and volume. Increasing expiratory times (sequences 6 and 7 compared with 3, 4, and 5) decreased lung pressure and volume. Increasing the airway diameter (sequence 8) had only slight effect on lung pressure and volume.(ABSTRACT TRUNCATED AT 250 WORDS)